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Human Immunodeficiency Virus HIV FAQs

Human Immunodeficiency Virus (HIV)

Human immunodeficiency virus (HIV) or AIDS (acquired immunodeficiency syndrome) virus, is a virus that causes defects in the human immune system. In 1981, the human immunodeficiency virus was first discovered in Central America. It is a lentivirus that infects cells of the human immune system, a type of retrovirus.
On October 27, 2017, the World Cancer Organization’s International Agency for Research on Cancer published a preliminary list of carcinogens. Human immunodeficiency virus type 1 (infection) is in the list of first-class carcinogens. In the list of category 2B carcinogen.

Scientific name:    Human immunodeficiency virus

Latin name:    Human Immunodeficiency Virus (HIV)

Nickname:    AIDS

Boundary:    Virology

Branch:    RNA Virus

Distribution Area:    Global

Table of Content

    1 Source

    2 Morphological characteristics

    ▪ Morphological structure

    ▪ Coding genes

    ▪ Virus characteristics

    3 Virus Development

    ▪ First Discovery

    ▪ Virus naming

    ▪ Virus status

    ▪ Antibody negative

    4 Survival conditions

    ▪ Survival in vitro

    ▪ Inactivation method

    ▪ Humoral survival

    5 Ways of infection

    ▪ Transmission

    ▪ Pathogenic mechanism

    6 Hideout

    ▪ Intestinal lymph nodes

    ▪ Memory T cells

    ▪ CD4 cells

    7 Testing methods

    ▪ Antibody testing

    ▪ Antigen detection

    ▪ Nucleic acid detection

    8 Training methods

    9 Main symptoms

    ▪ Suspected symptoms

    ▪ Asymptomatic latent

    10 Human damage

    ▪ Eroded cells

    ▪ Ignore antibodies

    ▪ Help cancer

    ▪ Take life

    11 Vaccine Development

    12 Research Progress

    ▪ Origin doubt

    ▪ Hijacking cells

    ▪ Virus antibodies

    ▪ Activate latency

    ▪ Remove virus

    13 Cure cases

What is the Source of HIV(Human immunodeficiency virus)?

On March 4, 2015, scientists from multiple countries found that the four known strains of HIV are from chimpanzees and gorillas in Cameroon. This is the first time that all sources of HIV strains have been fully identified.

There are four known HIV strains, namely M, N, O and P, each with a different source. Among them, the most widely spread M and N have long been confirmed to be from chimpanzees, but the rarer O and P are It was later confirmed that both O and P were gorillas from southwest Cameroon.

There are only two P-type cases in the world so far, and O-type is only 100,000, mainly in Central and West Africa.

Morphology of HIV Human Immunodeficiency Virus

What are the Morphological Characteristics of HIV (Human immunodeficiency virus)?

Morphology of HIV: The human immunodeficiency virus is approximately 120 nanometers in diameter and is roughly spherical. The outer membrane of the virus is a lipid envelope derived from the host cell and embedded with the viral proteins gp120 and gp41.

gp41 is a transmembrane protein, gp120 is located on the surface and binds to gp41 through non-covalent interactions. Inwards are a spherical matrix formed by protein p17 and a semi-conical capsid formed by protein p24.

The capsid shows a high electron density under an electron microscope.

 The capsid contains the viral RNA genome, enzymes (reverse transcriptase, integrase, protease) and other components from the host cell (such as tRNAlys3, used as primers for reverse transcription).

What is the Coding Gene of HIV (Human immunodeficiency virus)?

The viral genome is two identical positive-strand RNAs, each of which is approximately 9.2-9.8 kb in length.

The two ends are long terminal repeats (LTR), which contain cis-regulatory sequences to control the expression of the provirus.

It has been shown that LTR has promoters and enhancers and contains negative regulatory regions.
The sequence between LTRs encodes at least 9 proteins, which can be divided into three categories: structural proteins, regulatory proteins and accessory proteins.
1. The gag gene encodes a polymer precursor protein composed of about 500 amino acids, which is hydrolyzed by protease to form nuclear proteins P17 and P24, which protects RNA from damage by external nucleases.

2. The Pol gene encodes a polymerase precursor protein, which is cut to form a protease, an integrase and a reverse transcriptase (both having DdRp and ribonuclease H functions), all of which are necessary for virus proliferation.

3. The env gene encodes a precursor protein of about 863 amino acids and is glycosylated into gp160, gp120 and gp41. gp120 contains neutralizing antigenic determinants.
It has been proved that HIV neutralizes epitopes. 
On the gp120 V3 loop, the V3 loop is an important functional region of the envelope protein and plays an important role in the fusion of virus and cells. gp120 is linked to the transmembrane protein gp41 by a non-covalent bond. 
The fusion of gp41 with the target cell causes the virus to enter the cell. 
Experiments have shown that gp41 is also highly antigenic and can induce antibody responses.

4. The protein encoded by TaT gene can be combined with LTR to increase the transcription rate of all viral genes, and also can promote the translation of viral mRNA after transcription.

5. Rev gene product is a cis-activating factor, which can inhibit the cis-acting repression sequance (Crs) in env and gag, and enhance the expression of gag and env genes to synthesize corresponding virus structural proteins. .

6. Nef gene encoding protein P27 has a negative regulatory effect on HIV gene expression to delay virus replication. This protein acts on the LTR of HIv cDNA and inhibits integrated viral transcription. It may be necessary for HIV to maintain a sense of persistence in the body.

7. The Vif gene is not essential for HIV, but may affect free HIV infectivity, virion production, and in vivo transmission.

8. The VPU gene is unique to HIV-1, and is essential for effective replication of HIV and assembly and maturation of virions.

9. The protein encoded by the Vpr gene is a weak transcriptional activator and plays a role in the in vivo reproduction cycle.

HIV-2 gene structure is different from HIV-1: It does not contain VPU gene, but has a VPX gene of unknown function. 
Nucleic acid hybridization examined the nucleotide sequences of HIV-1 and HIV-2, which were only 40% identical. Env gene expression products stimulate the body to produce antibodies without cross-reactivity.

What are the Human Immunodeficiency Virus Characteristics?

The auxiliary T lymphocyte system mainly attacks the human body. Once it invades the body cells, the virus will integrate with the cells and will be difficult to eliminate for life.

It is widely present in the blood, semen, vaginal secretions, milk, cerebrospinal fluid and cerebral tissue fluids with neurological symptoms of infected persons, among which blood, semen and vaginal secretions have the highest concentrations.

The resistance to the external environment is weak, and the effective disinfection method for hepatitis B virus is also effective for HIV disinfection.

Infected persons have a long incubation period and a high mortality rate.

The genome of the AIDS virus is more complex than any known viral gene.

Development of HIV Human Immunodeficiency Virus

How Human Immunodeficiency Virus Development took place?

I.                  HIV Found

AIDS was first identified in the United States in the early 1980s and was ignored by Reagan’s conservative government.
However, with the continuous work of the US Centers for Disease Control and Prevention and knowledgeable doctors and scientists, conclusive epidemiological data has been accumulated, showing that AIDS has a certain infectious cause (etiology).

The infections caused by needles and blood transfusions have gradually increased, and many scientists have begun investigating this infectious agent.

II.               Virus Naming

French virologist Luc Montagnier  specializes in the relationship between retroviruses and cancer at the Pasteur Institute in Paris.

His research team first obtained from a young man with advanced Kaposi's sarcoma in 1983 A new retrovirus was isolated from the blood and lymph node samples of people living with HIV / AIDS.

They found that this virus is different from human T cell leukemia virus (HTLV) but a lentivirus (Lentivirus), they named it "Immune Deficiency-Associated Virus" (IDAV).

On the other side of the Atlantic, Montagne’s collaborator at the time, Robert Gallo, an American biomedical scientist at the National Cancer Institute, and his staff also isolated new viruses from some cell lines and named them Human III Cell Leukemia Virus-IIIB / H9 (HTLV-IIIB / H9).

Gallo's group first published a paper in the journal Science in 1984 to demonstrate this Relationship between new viruses and AIDS.

In 1986, the name of the virus was unified as "Human Immunodeficiency Virus" (HIV) to better reflect the nature of the virus that causes immunodeficiency rather than cancer.

III.            Virus Status

It has caused nearly 12 million deaths worldwide and more than 30 million people became infected.

On July 25, 1986, the World Health Organization (WHO) issued a communiqué, and the International Virus Taxonomy Committee decided to rename HIV as human immunodeficiency virus (HIV).

In 2004, an estimated 35.9 to 44.3 million people worldwide lived with human immunodeficiency virus, of which 4.3 to 6.4 million were new infections, and 2.8 to 3.5 million died of AIDS.

These numbers are constantly increasing, and among them, East Asia, Eastern Europe and Central Asia have the fastest growth. 

The worst-affected areas remain sub-Saharan Africa, followed by South and Southeast Asia.

IV.           Antibody Negative

Experts from the Department of Respiratory Medicine, Infectious Medicine, and Pathology of Peking Union Medical College Hospital jointly published the world's first case of HIV-negative AIDS combined with pulmonary Kaposi's sarcoma in the Journal of Clinical Respiration in November 2017.

The imaging and pathological characteristics of pulmonary Kaposi's sarcoma in this case are very typical. Peking Union Medical College's first diagnosis of pulmonary Kaposi's sarcoma through pathology in China is of groundbreaking significance and will help improve domestic doctors' understanding of the disease.

V.              What is the Survival Condition of Human immunodeficiency virus?

In vitro survival of HIV: It has extremely poor viability in vitro, is not resistant to high temperatures, has low resistance, and is difficult to survive without the human body.

 At room temperature, it can only survive for a few hours in the blood outside the body. It is sensitive to heat and loses its activity after 30 minutes at 56 , so it will not be infected in daily contact.

Inactivation method of HIV: When no stabilizer is added, the virus loses its activity under freezing at -70 .

While adding 35% sorbitol or 50% fetal bovine serum, it remains active after freezing at -70 for 3 months.

It is also sensitive to disinfectants and detergents. 0.2% sodium hypochlorite, 0.1% bleaching powder, 70% ethanol, 35% isopropyl alcohol, 50% ether, 0.3% H2O2 0.5% to Suer treatment for 5 minutes can inactivate viruses. 1% NP-40 and 0.5% triton-X-100 can inactivate the virus and retain antigenicity.

Strong resistance to ultraviolet rays and gamma rays
The International Health Organization recommends heating the inactivated HIV at 100 ° C for 20 minutes. The effect is ideal.

The disinfection of HIV is mainly aimed at medical supplies and living places contaminated by the blood and body fluids of people infected with HIV and AIDS patients. For example, accessories, gauze, clothing, etc.

For the disinfection of HIV, an appropriate physical method or chemical method can be selected according to the disinfected items. Items that need to be reused can be sterilized by boiling or high-pressure steam. Items that should not be boiled can be disinfected with 2% glutaraldehyde and 75% alcohol.

Humoral survival of HIV: At room temperature, HIV can survive for 15 days in a laboratory-controlled tissue culture fluid environment.

Some research institutes have proved that the survival time of HIV in isolated blood depends on the content of virus in the isolated blood.

 Blood with a high content of virus can still be viable even if it is left at room temperature for 96 hours without drying.
Even with a drop of blood at the tip of a needle, if fresh lymphocytes are encountered, HIV can still replicate in it and can still spread.

Blood with low virus content loses its vitality after 2 hours of natural drying out.

While blood with high virus content, even after drying for 2-4 hours, once placed in the culture medium, it can still enter lymphocytes and continue to replicate . But these situations are limited to the laboratory environment.

According to the American CDC report, even in a laboratory environment, viruses used in the laboratory for much higher concentrations than human blood and body fluids showed a 99% reduction in activity after drying for several hours.

Therefore, with the exception of the laboratory environment, the risk of infection with HIV-containing ex vivo blood is almost zero.

HIV cannot survive in the air, water and food, and these viruses will quickly die outside, even in blood and other body fluids containing HIV.
HIV Tests for Testing Human Immunodeficiency Virus

Not in a laboratory environment or in a closed environment (such as syringes and needles), HIV cannot maintain activity. It must be pointed out that in the residual blood of used injection needles.

HIV can survive for a relatively long time, and the needle can directly enter the blood of the human body. Therefore, used injection needles are very dangerous for HIV infection.

Used injections, the needle must never be reused. Relevant scientific research departments in the United States have obtained the results of nearly a million special-case exposure experiments excluding a clear transmission route: less than one in ten thousand cases of infection.
Infection Mode of Human Immunodeficiency Virus HIV

What is the Mode of Infection from HIV (Human Immunodeficiency Virus)?

Way for spreading of HIV: HIV-infected persons are the source of infection, and HIV has been isolated from blood, semen, vaginal fluid, and milk.

Shaking hands, hugging, kissing, swimming, mosquito bites, sharing tableware, coughing or sneezing, daily contact, etc. will not spread.

What are the 3 Main Modes of HIV Human Immunodeficiency Virus Transmission?

Sexual contact transmission

HIV exists in the semen and vaginal secretions of infected persons. Sexual behavior can easily cause subtle skin and mucous membrane damage, and the virus can enter the blood through the damage and become infected. 

Whether it is same-sex or heterosexual sexual contact will lead to the spread of AIDS. There are a lot of viruses in the semen or vaginal secretions of people with AIDS. 

During sexual activity (including vaginal sex, anal sex and oral sex), due to the friction of the sexual intercourse site, it is easy to cause slight damage to the genital mucosa.

 At this time, the virus will Take advantage of it and enter the blood of uninfected people.

 It is worth mentioning that because the rectal wall is more likely to break than the vaginal wall, the risk of anal sex is greater than that of vaginal sex.

Blood spread

Blood or blood products containing HIV, intravenous drug use, tissues and organs of infected persons or patients are all at risk of infection.

Mother-to-child transmission

Women infected with HIV can also pass the virus to the fetus during pregnancy and childbirth, and infected mothers can also pass the virus to breast-feeding children through breastfeeding.

Pathogenic mechanism

HIV selectively invades CD4 molecules, mainly T4 lymphocytes, monocytes, and dendritic cells. The CD4 molecule on the cell surface is an HIV receptor.

After binding to the CD4 on the cell membrane through the HIV envelope protein gp120, the conformation of gp120 changes to expose gp41. At the same time, gp120-CD4 binds to the chemokine CXCR4 or CXCR5 on the surface of the target cell to form CD4-gp120. -CXCR4 / CXCR5 trimolecular complex.

gp41 acts as a bridge in it, using its own hydrophobic effect to mediate the fusion of viral capsule and cell membrane. 
Eventually the cells are destroyed. 

The mechanism is not fully understood and may work in the following ways:
1. As HIV envelope proteins are inserted into cells or virus buds are released, cell membrane permeability is increased and osmotic lysis occurs.

2. The CD-gp120 complex in the infected cells is fused with the membranes of organelles (such as Golgi apparatus, etc.) to dissolve them, leading to the rapid death of infected cells.

3. Unincorporated DNA accumulation during HIV infection, or inhibition of cellular proteins, leads to HIV killing of cells.

4. The gp120 expressed by HIV-infected cells can bind to CD4 on the uninfected cell membrane, fuse under the action of gp41 to form multinucleated giant cells and dissolve to death.

5. HIV-infected cell membrane virus antigens bind to specific antibodies and lyse cells by activating complement or mediating ADCC effects.

6. HIV induces autoimmunity. For example, gp41 has a homology region with MHC class II molecules on the membrane of T4 cells. Anti-gp41 antibodies can cross-react with such lymphocytes, leading to cell destruction.

7. Programmed cell death: Apoptosis can be activated during the onset of AIDS. For example, gp120 of HIV binds to CD4 receptor. It directly activates the apoptosis of infected cells. 

Even the envelope antigen expressed by HIV-infected T cells can activate normal T cells, which indirectly causes a large amount of apoptotic CD + 4 cells to be destroyed by cross-linking of CD4 molecules on the cell surface, resulting in severe immune defects centered on T4 cell defects.

The patient's main manifestations: peripheral lymphocyte reduction, T4 / T8 ratio configuration, the response to phytohemagglutinin and certain antigens disappears, delayed allergic reaction decreases, the activity of NK cells and macrophages decreases, IL2, interferon gamma Reduces cytokine synthesis.

Early in the course of disease, because B cells are in a polyclonal activation state, the serum lg level in patients often increases. 

As the disease progresses, the function of B cells to produce antibodies to various antigens is also directly and indirectly affected.

People with AIDS suffer from severe immunodeficiency and often have severe opportunistic infections.
Common bacteria (mycobacterium intracellular avian complex, MAI), protozoa (pneumocystis carinii, toxoplasma) and fungi (candida albicans, Cryptococcus neoformans), viruses (cytomegalovirus, herpes simplex virus, hepatitis B virus), which eventually lead to uncontrollable death.

In other cases, Kaposis sarcoma or malignant lymphoma can occur.
In addition, HIV in infected mononuclear macrophages is proliferated at a low level without causing lesions, but damages its immune function, can spread the virus throughout the body, and causes interstitial pneumonia and subacute encephalitis.

After entering the human body, the AIDS virus was first engulfed by macrophages, but the AIDS virus quickly changed the acidic environment in certain parts of the macrophages, creating conditions suitable for its survival, and then entered a large number of T-CD4 lymphocytes.

Reproduction eventually destroys the latter immune cells completely.

HIV infection can stimulate the body to produce antibodies to envelope proteins (Gp120, Gp41) and core proteins (P24).
Low levels of antiviral neutralizing antibodies have been detected in the serum of HIV carriers and AIDS patients.
Among them, AIDS patients have the lowest levels and HIV carriers have the highest, indicating that the antibodies have protective effects in the body.

However, the antibody should not be in contact with the virus remaining in the mononuclear macrophage, and the HIV envelope protein is susceptible to antigenic mutation, and the original antibody will lose its function, so that the neutralizing antibody cannot play its due role.

During the latent infection phase, HIV provirus is integrated into the host cell genome, so HIV is not recognized by the immune system, so it cannot be cleared by relying only on its own immune function.
Hiding Place for HIV or Human Immunodeficiency Virus

Is there any Hiding place of HIV or Human Immunodeficiency Virus?

For a long time, the medical community discovered during clinical treatment that all HIV carriers receiving intensive treatment reappeared soon after the treatment was stopped, and inferred that not only the HIV hiding place exists in the body of the infected person The place, and the body's immune system is difficult to effectively control it.

Intestinal lymph nodes

After further research, scientists have found that T-CD8 lymphocytes (cytotoxin T lymphocytes) in the intestinal lymph nodes are less active. Such killer lymphocytes in other tissues can usually destroy infected cells and control the virus.
But the lymphocytes in the intestinal lymph nodes lack this ability, which causes the HIV to hide in it and gradually spread to other organs, making the disease worse.

Subsequently, the researchers confirmed that it is TGF-β cytokine that causes T-CD8 lymphocyte dysfunction in intestinal lymph nodes, and it is precisely that it inhibits the activity of T-CD8 lymphocytes, leading to premature aging.

French scientists say that their research provides new ideas for the complete defeat of AIDS, such as inhibiting TGF-β cytokines, repairing T-CD8 lymphocytes with impaired function, and strengthening treatment for intestinal lymph nodes. This will also be their next main subject.

Memory T cells

Memory T cells are a hiding place for some HIV viruses. When the cell is alive, the virus is alive. The cell dies and the virus is released, infecting more healthy cells.

Memory T cells, a type of human immune cell, although it is a hiding place for some HIV viruses, can also limit the activity of these viruses to a certain extent.

CD4 cells

HIV attaches to CD4 cells, reenters CD4 cells and infects it. When a person is infected with HIV, the virus creates more virus cells in the immune system of the infected person, turning it into a factory for making viruses.

 HIV will continue to replicate, CD4 cells will be destroyed, and the immune system will create new immune cells to replace dead immune cells, but the newly created immune cells will not be immune to HIV infection.

 Even if people living with HIV feel good and have no symptoms, at this time, hundreds of millions of CD4 cells may have been destroyed.

CD4 is the most important immune cell. Once an infected person loses a large number of CD4 cells, the entire immune system will be fatally hit, and will lose resistance to various diseases.

Detection Method of Hiding place of HIV or Human Immunodeficiency Virus

What is the Detection Method of HIV?

The method for detecting viral antigens and antibodies in body fluids of HIV-infected persons is convenient to operate and easy to popularize and apply, in which antibody detection is particularly common. However, the status and importance of HIv P24 antigen and viral genes in the detection of HIV infection have also received increasing attention.

Antibody detection

HIV antibodies in serum are an indirect indicator of HIV infection.

According to its main scope of application, existing HIV antibody detection methods can be divided into screening tests and confirmation tests.

HIV Confirming Reagents

Western blot (WB) is the most commonly used to confirm the positive serum of the screening test.

Because the method has a relatively long window period, a slightly lower sensitivity and a high cost, it is only suitable as a confirmation experiment.

With the improvement of the sensitivity of the third and fourth generation HIV diagnostic reagents, WB has been unable to meet its requirements for confirmation experiments.

Another type of screening confirmation reagent approved by the FDA is the immunofluorescence test (IFA). 
IFA is cheaper than WB, and the operation is relatively simple. The whole process can be completed in 1-1.5 hours.

The main disadvantage of this method is that it requires expensive fluorescence detectors and experienced professionals to observe the evaluation results, and the experimental results cannot be stored for a long time.

The FDA recommends that when a final result is released to a blood donor who cannot be determined by WB, the negative or positive of IFA shall prevail, but it shall not be regarded as a standard for blood qualification.

Screening Test for HIV

The screening test is mainly used for screening blood donors, so it requires simple operation, low cost, and sensitivity and specificity. 
In 2012, the main screening method in the world was still ELISA, as well as a few particle agglutination reagents and rapid ELISA reagents.

ELISA has high sensitivity and specificity, and is easy to operate. It only needs to be equipped with a microplate reader and a plate washer in the laboratory. 
It is especially suitable for large-scale screening in the laboratory.

The particle agglutination experiment is another simple and convenient, low-cost detection method.

The results of this method can be judged by the naked eye, and the sensitivity is very high.

It is especially suitable for developing countries or a large number of blood donors. Sex is poor.

Dot-blot assay developed in the late 1980s is a rapid ELISA (Rapid ELISA) method. This method is extremely simple to operate and the process is short. 
The entire process is mostly within 5-10 minutes or even 3 minutes. It can be ended, but this method is much more expensive than ELISA and particle agglutination reagents.

Human immunodeficiency virus antibody oral mucosal exudate detection kit (colloidal gold method) belongs to the category of lateral immunochromatography (gold immunoassay).

Based on immunochromatography technology, the results can be read manually and visually.

 A rapid diagnostic reagent with qualitative test results for the detection of HIV-1 and HIV-2 antibodies in oral mucosal exudate samples. 
It can be used for the initial screening of patients with voluntary consultation and testing, unwilling to collect blood and dizzy needles. 
This method is suitable for the initial screening test. Anyone who is tested positive by this reagent needs further screening confirmation.

[HIV negative] means that no HIV antibody can be detected from the human body, and the negative symbol is indicated by (-).

 It cannot be said that there is no HIV infection, depending on when it is detected.

During the window period, the infected person has not yet produced HIV antibodies, or sufficient HIV antibodies have not been produced. At this time, the HIV test is negative. 
Testing after the period can exclude the possibility of HIV infection.

[HIV positive] indicates that HIV antibody has been detected from the human body, and the positive symbol is indicated by (+).

What are the Uncertain factors of HIV Test Results?

Infection is still in the window period: The time from HIV entering the body to detection is not long enough, so the serum has not formed a typical antibody response.

AIDS progresses to end stage, antibody levels drop.
Cross-reactions of other non-viral protein antibodies. In autoimmune diseases, certain malignant diseases, pregnancy, blood transfusions, or organ transplants, the body can produce some antibodies, and the response is similar to that caused by the HIVP24 core protein antibody

Antigen Detection

Pathogen detection mainly refers to the direct detection of viruses or viral genes from host specimens by methods such as virus isolation and culture, electron microscope morphological observation, virus antigen detection, and gene determination.

Because the first two methods are difficult which require special equipment and professional technicians. Therefore, only antigen detection and RT-PCR (reverse transcription-PCR) can be used for clinical diagnosis.

HIV-1P24 antigen test can be used for auxiliary diagnosis of HIV-1 antibody indefinite or window period.

Eearly auxiliary differential diagnosis of infants born to HIV-1 antibody-positive mothers.

Fourth-generation HIV-1 antigen / antibody ELISA reagent test is positive However, HIV-1 antibody confirmed negative diagnosis. P24 antigen detection generally uses ELISA double antibody sandwich method reagents.

The reagents must be registered and approved by SDA. Within the validity period, the positive results must be confirmed by neutralization test according to the reagent instructions. 
The sensitivity of the HIV-1P24 antigen test is 30-90%.
This result is only used as a supplementary diagnostic basis for HIV infection and cannot be diagnosed accordingly.

A negative HIV-1 P24 antigen test only means that there is no response in this test, and HIV infection cannot be ruled out.  Generally it is not used as a routine diagnostic item in clinical practice.

Nucleic Acid Detection

HIV nucleic acid testing can be used for auxiliary diagnosis of HIV infection, monitoring of disease course, guiding treatment plan and judgment of curative effect, predicting disease progress, etc.

Commonly used HIV viral load detection methods include reverse transcription PCR (RT-PCR), nucleic acid sequence amplification experiment (NASBA), branched DNA hybridization experiment (bDNA), and real-time fluorescent quantitative PCR technology.

 It is worth noting that each HIVRNA quantification system has its minimum detection limit, that is, the lowest copy number or international unit that can be measured. 

When the RNA is not detected during quantitative detection, it does not mean that the sample does not contain viral RNA, so the HIV nucleic acid is qualitative. 
If the test is negative, only the negative result of this experiment can be reported, but HIV infection cannot be ruled out.

HIV nucleic acid test is positive, it can be used as an auxiliary indicator for diagnosis of HIV infection, and cannot be used alone for the diagnosis of HIV infection.

When reporting HIV nucleic acid quantitative test results, report the results according to the instrument reading, indicating the experimental method used, the type of sample, and the amount of the sample.

When the measurement result is less than the minimum detection limit, indicate the minimum detection limit level.

Qualitative detection of HIV nucleic acid can also be used as an auxiliary diagnosis of HIV infection, and it can be used in basic research such as analysis of HIV genotypes and mutations. 
Usually PCR or RT-PCR technology is used, and the amplification reagents commonly used in molecular biology laboratories are used.

 The primers can be from the literature or designed by themselves. They should cover all or common strains as much as possible. Compound primers can also be used.

When reporting qualitative test results, the reaction conditions and primer sequences used should be noted. In addition, using the high sensitivity of nucleic acid detection methods, using collective nucleic acid amplification detection techniques and methods, collective nucleic acid detection can be performed on samples that are highly suspected to be infected and antibody-negative samples can detect window-infected patients in a timely manner.

This method is more cost-effective than nucleic acid detection in a single sample.

Training method

The common method is the co-culture method, that is, the mononuclear cells are isolated from the peripheral blood of normal people, stimulated and cultured with PHA. 
These cells are then added to the diagnosis of patients' mononuclear cells and the study of AIDS.

The lymphocytes in the patient's own periphery or bone marrow are stimulated by PHA for 48 to 72 hours for in vitro culture (IL2 is added to the culture medium) for 1 to 2 weeks, the virus proliferation can be released outside the cell. 
The cells are fused into multinucleated giant cells. The cell ruptured and died.

Passive lymphocyte lines such as HT-H9 and Molt-4 cells can also be used for isolation and passage.

HIV animals have a narrow range of infections, and only chimpanzees and gibbons are commonly used for experiments. 
Infect chimpanzees with HIV-infected or cell-free HIV filtrates, or infuse HIV-infected chimpanzee blood to normal chimpanzees, and the infection is successful.
Continue to isolate HIV in the blood and lymph fluid for 8 months, after 3 to 5 weeks Find HIV-specific antibodies and continue to maintain a certain level. But neither chimpanzee nor gibbon infected after the disease.
Symptoms of Hiding place of HIV or Human Immunodeficiency Virus

What are the main Symptoms of HIV (Human Immunodeficiency Virus)?

Suspected symptoms

Common symptoms

Persistent extensive lymphadenopathy, especially cervical, axillary, and groin lymph nodes. 
Lymph node enlargement is about 1 cm in diameter, hard, painless and mobile, and lasts more than three months.
1. Unexplained fever and night sweats for several weeks.

2. Severe fatigue that has been unexplainable for weeks.

3. Appetite loss, weight loss in more than 10% of original weight within 2 months.

4. Chronic diarrhea of ​​unknown cause has appeared for several weeks, showing a watery pattern, more than 10 times a day.

5. Shortness of breath, dry cough for several weeks.

6. Flat and raised pink and purple-red spots appear on the skin and mouth without pain or itching.

7. White spots appear in the pharynx and larynx. T
here are scaly patches and itching in the male genitals. 
Women have anal itching, vaginal itching, and leucorrhea.

8. Headache and blurred vision.

When more than the above three symptoms and a history of unclean sexual contact, should go to the hospital for examination.

The symptoms caused by the HIV virus are not specific. In real life, there are many reasons that can cause the above symptoms. 
You cannot conclude that you have the HIV virus because your body has related symptoms. 
Only a scientific "HIV antibody / antigen test" can draw a correct conclusion.

Asymptomatic latent

Some people have been asymptomatic after HIV invaded the body, and went directly to the asymptomatic period. 
The length of AIDS incubation period varies greatly between individuals, which may be related to the type, intensity, quantity, infection route of the invading  AIDS virus and the immune function, health status, nutritional status, age, life and medical conditions, psychological factors of the infected person.
It is generally 6-10 years, but about 5-15% of people progress to AIDS within 2-3 years, called rapid progressers.

5% of patients whose immune function can maintain normal for more than 12 years, Called long-term non-progressors.

Human damage

HIV not only makes it difficult for the body's immune system to resist its invasion, but also makes it difficult for the development of special therapeutic drugs and preventive vaccines.
HIV directly invades the body's immune system and destroys the body's cellular and humoral immunity.
It is mainly found in the body fluids of infected people and patients (such as blood, semen, vaginal secretions, breast milk, etc.) and in many organs.
It can be transmitted through HIV-containing body fluid exchange or organ transplantation.

Erosion cell

HIV has been proven to be a T4-lymphocyte and neuroblast virus. HIV enters the body's blood from a broken skin or mucous membrane, and mainly attacks and destroys the target cell T4 lymphocytes (T4 lymphocytes play a central regulatory role in the cellular immune system, which can promote B cells to produce antibodies), and T4 cells are lost The original normal immune function.

When almost all of the T4 cells that activate the immune response are eliminated by HIV, the number of T4 cell suppressor cells increase dramatically.

On the contrary, the number of T4 cells in the patient's body decreases suddenly, which leads to the total failure of the patient's immune function, creating an extremely extreme favorable conditions.

HIV has an affinity for nerve cells, can invade the nervous system, cause the destruction of brain tissue, or cause a variety of central nervous system lesions due to secondary conditioned infection.

Ignore antibodies

After entering the human body, the AIDS virus was first engulfed by macrophages, but the AIDS virus quickly changed the acidic environment in certain parts of the macrophages, creating conditions suitable for its survival, and then entered a large number of T-CD4 lymphocytes.

Reproduction eventually destroys the latter immune cells completely.

HIV envelope proteins are prone to antigenic mutations, and the original antibodies lose their effect, making neutralizing antibodies unable to play their due role.

During the latent infection stage, the HIV previrus integrates into the host cell's genome.

The immune system ignores HIV and does not recognize it by the immune system. Autoimmunity cannot be eliminated.

The human immune system has the ability to suppress early HIV. Recent studies have shown that most newly infected patients develop neutralizing antibodies. 
These antibodies are droplet-shaped blood proteins that attach to the virus. If they face only one target, they allow patients to defend themselves.

But the problem is that HIV has the ability to mutate. Its ability to disguise itself is enough to escape the pressure of antibodies. 
HIV will eventually disintegrate the immune system and deplete it. Some AIDS viruses can mutate some of the outer protein.

After the mutation, an enzyme may attach a sugar molecule to it and interfere with the attack of the antibody. But this "glycan shield" phenomenon cannot be observed in all cases.

Other viruses mutate parts of the outer layer of proteins that are directly attached by neutralizing antibodies.

HIV-1 invades immune system cells called T-lymphocytes, "hijacks" the "molecular machinery" of T-lymphocytes to make more HIV-1. Then it ultimately destroys host cells-which makes infected people more vulnerable to other lethal diseases Impact of the disease.

However, T lymphocytes are not easy to be hit by. Within their anti-virus defense system is a class of proteins called APOBEC3s, which has the ability to prevent HIV-1 from replicating itself.

However, HIV-1 also has an anti-defense mechanism-a protein called virion infection factor (Vif), which can cause T lymphocytes to destroy their own APOBEC3s.

Helps develop cancer

HIV is similar to other retroviruses. When reverse transcriptase synthesizes DNA from viral RNA as a template and integrates the viral DNA into the DNA of the host cell, the oncogenes carried by HIV can cause the cancerous transformation of cells.
Especially, under the circumstance that the cellular immunity is destroyed and the immune surveillance function is lost, the change of cell carcinoma is easy to occur.

Take life

The survival time of AIDS patients has a great relationship with the type of subtype virus they are infected with.

The average survival time of AIDS patients varies greatly depending on the type of subtype infected, although the number of viruses infected by these subjects is basically the same.

The average survival time of those infected with subtype A virus was 8.8 years, while the average survival time of those infected with subtype D virus was reduced to 6.9 years.

 The survival time of those with mixed infection of subtype D and subtype A viruses was shorter. The average is only 5.8 years.
Vaccine Development for Human Immunodeficiency Virus HIV

What is going on about HIV Vaccine Development?

In September 2009, a medical trial supported by the US military in Thailand found that an experimental vaccine can greatly reduce the risk of contracting HIV. 
For the first time, humans have received an AIDS vaccine with a certain immune effect.

What are the Challenges in the development of an HIV-1 Vaccine?

  1.  Extensive Viral class & sequence diversity
  2.  Early establishment of latent viral reservoirs
  3.  Immune correlates of protection unclear
  4.  Viral evasion of humoral and cellular immune responses
  5.  Anti-body responses typically type-specific
  6.  No method exists to elicit broadly reactive neutralizing antibodies
  7.  Attenuated viruses unsafe for human use
  8.  Lack of small-animal model
  9.  Little pharmaceutical interest

  1.  Wide range of viruses and sequence diversity
  2.  Early establishment of latent viral reservoirs
  3.  Unclear immune-related protection
  4.  Viral escape of humoral and cellular immune responses.
  5.  Typical anti-body response
  6.  No existing method to cause widespread reactive neutralizing antibodies
  7.  The attenuated virus is not safe for human use
  8. Lack of small animal models

Vaccine development Challanges for HIV-1 vaccine

What are the Challenges in the Development of HIV-1 vaccine?

Little Medical Gains

Scientists performed a nearly full-length genome analysis of HIV-1 on a Burmese long-distance trucker in the border area between China and Myanmar, and found that the HIV-1 CRF01_AE / B / C recombinant virus strain was more than the HIV recombinant virus reported from Myanmar 12 years ago. The strain is more complicated. 

"Human immunodeficiency virus" (English abbreviation HIV) can destroy the body's immune system after invading the body, causing the body to produce a variety of incurable infections and tumors, which eventually lead to death.

It has been confirmed that HIV is divided into two types: HIV-1 And HIV-2. Worldwide, HIV-1 infection predominates.

What is the Research Progress regarding Human Immunodeficiency Virus - HIV?

HIV Origin Doubt

With the continuous deepening of HIV research, people have isolated monkey immunodeficiency virus similar to HIV, referred to as SIV, in different primates. 
SIV and HIV are basically the same in gene size and composition, but SIV does not cause any disease in its natural host monkey.
However, when SIV isolated from a natural host is inoculated into an unnatural host monkey, it will cause symptoms similar to human immunodeficiency.
For example, after inoculating SIVsm isolated from Florida rhesus monkeys to rhesus monkeys, after a clinical incubation period, they will produce clinical symptoms similar to AIDS, such as diarrhea, weight loss, and imbalanced CD4 and CD8 cells.

It has also been found that the genetic variation of viruses isolated from wild African green monkeys is very large, and this variation is consistent with the evolutionary relationship of different species of monkeys, suggesting that monkey immunodeficiency viruses have co-evolved in monkeys for quite a long time.

 All these studies suggest that human HIV may be transmitted from monkeys to humans in the form of cross-transmission between different species.

Until the early 1990s, Gao Feng and Hahn and others in the study of the epidemic of HIV-2 in remote areas of Africa provided a more direct clue to the origin of HIV, which further proved that Type B HIV originated in monkey HIV.

 The most important finding of the study was the isolation of a virus (HIV-2 / FO784) similar to monkey immunodeficiency diseases SIVsm and SIVmac from an HIV-2 healthy carrier.

 In evolutionary analysis, due to the high homology between FO784 and SIVsm / mac, they cannot be distinguished from each other in the evolution tree, which strongly suggests that human HIV originated from monkey immunodeficiency virus.

This was not only confirmed by later similar experiments, but also a large number of epidemiological results also supported this conclusion.
i.                  About 30% of wild Florida monkeys are infected with SIVsm. A large proportion of wild monkeys carry SIV, which directly proves that the Florida long-tailed monkey is the natural host of SIVsm.
ii.               SIVsm and HIV-2 co-exist in the same geographic area in several countries in western Africa. And people living together in West Africa have close contact with the Florida vervet monkeys. For example, people often hunt Florida vervet monkeys as pets or food.
iii.            Florida cynomolgus monkeys infected with SIVsm do not produce any clinical symptoms, but when SIVsm is inoculated into rhesus monkeys, it produces immune deficiency syndrome similar to humans. All of this shows that SIVsm and Florida monkeys have formed a symbiotic relationship, that is, Florida monkeys have become the natural host of SIVsm, and no longer have any clinical symptoms due to SIVsm infection. However, when SIVsm infects a new host, it causes clinical manifestations not found in its natural host. As with SIVsm infected rhesus monkeys, when SIVsm infects a new host human, immunodeficiency syndrome develops in the infected person. Therefore, human immunodeficiency syndrome is actually an animal infectious disease, that is, a disease that is transmitted from animals to humans in the natural state.

Of course, the most complete proof should be to obtain a large amount of epidemiological and genetic evidence for the direct transmission of SIVsm from the Florida monkey.
However, under the premise that this information is almost impossible, the isolation of SIV-like virus from humans provides the most convincing evidence that HIV originated from monkey HIV.

The subtypes D and E of HIV-2 are closely related to their corresponding SIVs, and form the same group with the corresponding SIVs in evolutionary analysis, but they cannot be distinguished from SIVs.
This shows that at least D and E are caused by the second independent transmission from monkey to human.
At least 5 different HIV-2 subtypes have been discovered in 2012, suggesting that this transmission between different species may have occurred at least 5 times for HIV-2.
Not long ago, in an accident, an experimenter was infected with SIV because he did not strictly observe the experimental operation regulations.

In the follow-up investigation for more than two years, the virus and corresponding antibodies were successfully detected from the experimenter's body, indicating that the experimenter has been infected by SIV.
The accident directly demonstrated the possibility of the transmission of immunodeficiency virus from monkeys to humans.

Through the above research, we have a relatively clear conclusion on the origin of HIV-2. However, the origin of HIV-1 has always been an unsolved mystery.

Although it is widely believed that HIV-1 originates from similar monkey viruses as HIV-2, clear evidence has been lacking.

Although a virus similar to human HIV-1 (SIVcpz) has been successfully isolated in chimpanzees, the genetic material between the two is very different.

Unlike the relationship between HIV-2 and SIVsm / mac, in the analysis of genetic evolution, HIV-1 does not form a closely related group with any SIVcpz. In addition, under natural conditions, the infection rate of chimpanzees is very low.

Of the hundreds of screened chimpanzees, only four were found to be serologically positive, which is well below the natural infection rate of SIVsm.

There are two views on the origin of HIV-l:

One view is that human HIV originated in SIVcpz, but SIVcpz samples that are closely related to HIV-1 have not yet been collected. However, due to the very low natural infection rate of chimpanzees, this is unlikely.

Another view is that humans and chimpanzees share a common source of HIV infection.
 However, the latest experimental results show that human HIV type I virus actually originated from chimpanzees in Africa.

 By analyzing the mitochondria of chimpanzee hosts and the SIV virus gene sequences they infected, the study proved that two of the four types of chimpanzees living in Africa were infected by their corresponding SIVs.

 All the current popular HlV-l originated from only one type of chimpanzee living in Central and West African countries. 
At the same time, in July 2009, scientists discovered that HIV can cause chimpanzees to die in large numbers.

A scientific research result of a team of young professor Hou Wei from the Wuhan University School of Basic Medicine and Professor Huo Wenzhe from the Animal Experiment Center of Wuhan University was published in August in the famous American academic journal "Lymphocyte Biology". The study found that a type of T lymphocyte that expresses the CD56 molecule has an anti-HIV infection effect.

After three years of research, it was first discovered that the secretion in the culture medium of "T-lymphocytes expressing CD56" can inhibit HIV infection and replication, and this activity has a broad spectrum, which can inhibit HIV stored in the laboratory. Strains can also inhibit clinically isolated HIV strains.
Although the secretions in the culture solution have little effect on the co-receptors of HIV entering the cells, they can enhance the effect of interferon regulatory factors, thereby causing macrophages to function and "fight against" HIV.

How HIV has spread in the population at an alarming rate in the past decade has not been clearly answered. However, due to the continuous development of the economy and the development of transportation, population mobility has greatly increased, and changes in living habits have undoubtedly played an important role in the epidemic of AIDS.

Hijack cell

In January 2014, Huang Zhiwei's research group at the School of Life Sciences of Harbin Institute of Technology revealed the structure of the HIV virion factor Vif for the first time in the world.
It clarified how Vif "hijacks" the molecular mechanism of human immune cells, and provided a structure for the development of new AIDS drugs basis.

 This research is of great significance and important scientific application value for mankind to finally overcome AIDS.

As a vital influencing factor in the nine major genes of HIV, Vif is considered by the academic community to be evolved against human evolution during the transmission of HIV. It degrades the virus in human immune cells by "hijacking" the protein degradation system in human immune cells.

Restriction factor members of the APOBEC3 family, thus evading immune cells' recognition and defense against HIV. But for a long time, no progress has been made in the analysis of the atomic level structure of Vif itself or its functional complexes.

In the research, Huang Zhiwei's research group focused on the "stubborn disease" of Vif, focusing on the analysis of the structure of the five-component complex of Vif, and described in detail how Vif "hijacks" the human CBF-β and CUL5 E3 ligase complex molecular mechanism.

This study analyzes the structural characteristics of HIV and understands how HIV is combined with people, which provides the possibility of further solving the problem of AIDS treatment.

According to the "key-on-key" rule, the study has also opened up a new path for future AIDS treatment from a "cocktail-style" mixed drug approach to the design of targeted therapeutic drugs.

The research paper has been published online in the journal Nature, and was featured in the "News and Perspectives" column of the journal Nature as a featured article.

Virus antibody

The National Institute of Infectious Diseases (NICD) in South Africa says scientists are looking for antibodies that can kill different strains of the virus (HIV) and are expected to develop AIDS vaccines.

Morris, director of the NICD's virology department, said scientists took a woman's blood sample to study her response to HIV infection and isolated the antibodies she produced.

The human body's response to HIV is to produce antibodies against the virus. In most cases, antibodies cannot neutralize or kill different virus strains, but a few broad-spectrum neutralizing antibodies can pass through the protective layer around HIV to kill the virus.

Moore, a scientist involved in the research, said that researchers have been able to replicate antibodies and will test whether they can exert immune functions without human infection.

She said: "We will carry out the monkey experiment first, and then we will start the human experiment." The human experiment will take at least 2 years.

Activation latency

Scientists from the Gladstone Institute report in the journal Science that they have found a new way to expose latent HIV to themselves, which may help overcome one of the biggest obstacles to finding a cure for HIV infection.
They found that without increasing the average level of HIV gene expression, as long as the random activity (noise) associated with HIV gene expression is increased, latent HIV can be reactivated.

 When HIV infects immune cells, it inserts its own genetic material into the DNA of infected cells. In most cases, the machinery of immune cells copies the genetic material of the virus, eventually resulting in the expression of all the elements needed to generate more viruses. New viruses are released from infected cells and will spread to other immune cells in the body.

However, in some cases, HIV expression enters a waiting mode, and the virus in the infected immune cells enters a latent state. This means that a small percentage of HIV is hidden in infected cells, and even the most effective drugs cannot reach them.

Method of Removing Human Immunodeficiency Virus - HIV form Human Cells

What is the Procedure to Remove Human Immunodeficiency Virus - HIV form Human Cells?

In July 2014, researchers in Philadelphia, the United States, discovered a way to completely remove HIV from human cells.
In a study published in the National Science Academic Progress Journal, the researchers first called a method called the nuclease's DNA cleavage enzyme binds to a target strand called ribonucleic acid, and then the combination begins to hunt down and eventually remove the HIV-1 viral genome.
After the removal, the cell's genetic repair program began to take over the entire process, welding the damaged ends together, resulting in a virus-free cell.

Because the HIV-1 virus cannot be cleared by the immune system, the disease can only be cured by removing the virus. These molecular weapons can also be used as vaccines. Cells armed with nuclease-ribonucleic acid have been shown to be immune to HIV infection.

The laboratory used a 20-nucleotide chain-directed ribonucleic acid to target the HIV-1 virus, and then used a DNA cleaving enzyme called Cas9 to modify the human genome. Researchers have come up with different strategies to apply to preclinical research, hoping to eliminate every HIV-1 virus in patients in order to cure AIDS.

Cure Case

On March 6, 2019, it was reported that a man with HIV in the British capital received a bone marrow transplant three years ago, "inheriting" the genetic mutation of the donor. He also did not detect HIV for more than 18 months, and is expected to become a follow-up patient "After the second successfully cured AIDS patient.

Author's Bio

Doctor Shawna Reason, Virologist
Dr. Shawna Reason
Name: Shawna Reason

Education: MBBS, MD

Occupation: Medical Doctor / Virologist 

Specialization: Medical Science, Micro Biology / Virology, Natural Treatment

Experience: 15 Years as a Medical Practitioner

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