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Herpes Virus Infections Biological Traits Immunity and Pathogenicity

Infections Biological Traits Pathogenicity of Herpes Virus

Herpes simplex virus (HSV) is a typical representative of herpes virus. It is named because herpes simplex occurs in the acute phase of infection. 

It can cause a variety of human diseases, such as gingivostomatitis, keratoconjunctivitis, keratoconjunctivitis, encephalitis, and reproductive system infections and newborn infections.

After infecting the host, a latent infection is often established in nerve cells. After activation, asymptomatic detoxification will occur. The chain of transmission will be maintained in the population and it will circulate repeatedly.

Scientific name:    Herpes simplex virus

Latin scientific name:    Herpes simplex virus

Boundary:    Virology

Branch:    Herpesviridae

Yaco:    Herpes alpha subfamily

Genus:    Herpes simplex virus

Table of Content

    1. Introduction

    2. Typing

    3. Biological traits

    4. Pathogenicity

    ▪ Primary infection

    ▪ Latent and recurrent infections

    ▪ Newborns and congenital infections

    ▪ Relationship with cervical cancer

    5 Immunity

    6. Pathogenic mechanism

    7. Detection

     ▪ Microbiological examination

    ▪ Nucleic acid amplification experiment

    ▪ Serum antibody test

    8. Prevention principles

HSV-1 is a circular virus synthesized by the envelope, capsid, core, and capsule. Double-stranded linear DNA synthesis is the focus of the virus. 
The filaments are wound in coils, ranging from 125 to 240 kb. 
The genome of HSV-2 is around 154kb. 
The G + G component in the genome of HSV-2HG52 strain is about 70%, and the middle part is synthesized by 18% short and 82% long fragments covalently connected at the LS border. 
Each fragment contains inverted repeats at both ends and a special middle part. Sequences, due to their different forms of connection, HSV-2 genome produces 4 isomeric molecules.
HSV has a variety of transcriptional regulation methods, complex genome structure, many genes and overlapping each other. The HSV-2 gene is transcribed and expressed through strict cascade regulation.
It is divided into three categories according to the time sequence:

  1. Immediate early genes
  2. Early genes
  3. Late genes


According to the difference in antigenicity, HSV is divided into two serotypes, HSV-1 and HSV-2. The DNA of the two types of viruses is 50% homologous, with common antigens and type-specific antigens.

Biological Traits of Herpes Virus

The virus is spherical and has an envelope with 11 envelope glycoproteins on its surface.

HSV-1 morphology

HSV has two serotypes, HSV-1, and HSV-2. 
The genomes of the two types are 50% homologous. They are composed of two linear DNA molecules with short and long segments connected by covalent bonds. 
HSV can proliferate in a variety of cells, and virus is usually isolated and cultured from primary rabbit kidney cells. 

Cytopathic effects occur shortly after cell infection, manifested by cell swelling and fusion with each other to form multinucleated giant cells and the production of eosinophilic intranuclear inclusions, which eventually lead to cell shedding and death. 
HSV animals have a wide range of infections. 
Commonly used experimental animals are rabbits, guinea pigs and mice.


Human is the natural host of herpes simplex virus. Infection is extremely common in the population. 80% -90% of the initial infections are recessive infections, most of which have no obvious symptoms, and a few of them are dominant infections. 
After the initial infection, it is often turned into a latent infection, which can cause recurrence after external stimuli.

The source of infection is patients and carriers and the route of transmission is direct or sexual contact. 

The virus can initiate infection by damaging the skin and mucous membranes. 
In addition, HSV-1 and HSV-2 may be related to lip cancer, vulvar cancer, and cervical cancer, respectively.

Primary infection of Herpes Virus

Primary infections occur in infants and preschool children aged 6 months to 2 years. The primary infection is usually confined to the oropharynx.
The virus is transmitted through the respiratory tract or directly on the saliva of the patient, causing chewing gum, manifested as fever, sore throat, clusters of herpes on the gums and cheeks, and ulcers after the herpes breaks. 
A large number of viruses are concentrated in the lesions.
In addition, the virus can also cause diseases such as herpes keratoconjunctivitis, cold sores, herpes encephalitis, and skin herpes eczema.

The primary infection of HSV-2 is mainly through sexual transmission, which causes genital herpes, which manifests as blisters in the genital area and ulcers after rupture.
Complications include extragenital damage and aseptic meningitis. A few primary infections can also be caused by HSV-1.

Latent and recurrent Infections of Herpes Virus

After the primary infection of HSV, the body's specific immune system will clear most of the virus and alleviate the symptoms. 

The unremoved virus reaches the sensory ganglia through sensory nerve fibers and stays in the nerve cells for a long time. 

The virus does not replicate. It causes clinical symptoms and insensitivity to antiviral drugs.
HSV-1 lurks in the trigeminal ganglia and superior cervical ganglia.
HSV 2 Herpes Virus Infections and Biological Traits

HSV-2 lurks in the phrenic ganglia. When the body is stimulated by fever, axonal damage, physical or emotional stress, certain bacterial or viral infections, sun exposure or the use of various non-specific factors such as adrenal corticosteroids,
the virus can be activated and travel along sensory nerve fibers to peripheral nerve.

The inner skin and mucosal epithelial cells re-proliferate, causing recurrence of local herpes. 
Recurrence is usually at the same site as the original infection, and because the body's immune response restricts virus replication, recurrent infections generally have shorter durations, more limited infection lesions, less tissue damage, and can be detoxified without symptoms. 

The latent form of HSV-1 exists in more than 80% of the population, but only a small number of people relapse and the mechanism is still unclear.

Neonatal and congenital infections of Herpes Virus

If pregnant women have HSV-1 infection, the virus may infect the fetus through the placenta, causing miscarriage, premature birth, stillbirth or congenital malformations. 

If a pregnant woman suffers from genital herpes, if the fetus touches the infected site in the birth canal during childbirth, local skin and oral lesions may occur, neonatal herpes occurs and severe cases of systemic symptoms or encephalitis. 75% of neonatal herpes caused by HSV- 2 causes.

What is the Relationship of Herpes Virus with cervical cancer?

HSV-2 infection is closely related to the occurrence of cervical cancer. Studies have shown that patients with cervical cancer have a high positive rate of anti-HSV-2 antibodies. Women with genital herpes have a significantly higher incidence of cervical cancer.

Anti-HSV infection Immunity

In anti-HSV infection immunity, neutralizing antibodies generally appear about one week after the primary infection and can last for many years.
This antibody can neutralize free viruses and reduce the severity of the disease, but it cannot prevent the virus from migrating to ganglion cells.
Also, it cannot clear the virus that is latent in the cells, and prevent the recurrence of the infection. Specific Tc cells appeared in the second week of HSV infection, destroying the host cells infected by the virus and clearing the virus. HSV has partial cross immunity between the two types.

Primary herpes simplex virus infection occurs in infants and young children from 6 months to 3 years of age, and about 70% to 90% of adults have HSV-1 antibodies. HSV-2 antibodies gradually increased with sexual maturity. 

About one week after the primary infection, neutralizing antibodies (IgM, IgG, IgA) appeared in the blood. Severe primary or recurrent infections have increased antibody levels. These antibodies cannot prevent reinfection or the recurrence of latent virus, but they can reduce the severity of the disease.
Pathogenic Mechanism of HSV

Pathogenic Mechanism of HSV

HSV-2 virus is the main cause of genital herpes. Once infected, patients will carry the virus for life and periodically develop genital herpes damage. 

HSV-2 infection will also increase the risk of HIV-1 transmission and is not targeted at HSV- An effective vaccine for 2 was launched. 

Due to the high positive rate of HSV-2 and the common transmission route with HIV-1, more and more attention has been paid to related research on HSV-2.
Previous studies have shown that HSV-2 must inhibit host cells' antiviral type I interferon (IFNα / β) signaling pathways to establish persistent infections, but the mechanism is unknown.
Research by the Hu Qinxue Group of the Wuhan Institute of Virology, Chinese Academy of Sciences found that HSV-2, through its very early protein US1, inhibits the production of IFN-β and evades the host's natural immune control.

This discovery provides a new mechanism for how double-stranded DNA virus families block the type I IFN signaling pathway.

It is difficult to establish long-term effective memory immune protection against HSV-2 in the genital tract mucosa, which has become a major bottleneck in the development of herpes virus vaccines. 

The Hu Qinxue group used the chemokine CCL19 to target and recruit immune cells to secondary lymphoid organs and mucosal tissues. 

The candidate immunogen HSV-2 gB protein and CCL19 were used as a chimeric DNA vaccine.

It was found that the "gB-CCL19" chimeric vaccine can induce good protection in mice, thus laying a foundation for designing vaccines against HSV-2 or other sexually transmitted viruses.

Detection of HSV

Microbiological examination: Can collect blister fluid, cerebrospinal fluid, saliva

HSV-1 structure

Vaginal swabs and other specimens were inoculated into susceptible cells such as human embryonic kidney, human amniotic membrane, or rabbit kidney. 
After 2 to 3 days of culture, cytopathic changes were observed. HSV isolates are usually identified and typed by immunohistochemical staining. 

Detection of HSV DNA in specimens by in situ nucleic acid hybridization or PCR has high sensitivity and specificity.

What is Nucleic acid amplification experiment?

Herpes simplex virus nucleic acid amplification assays (NAATs) have become a highly sensitive method for confirming herpes infection. 

Clinical specimens include genital ulcers, mucosal epidermal sites, and cerebrospinal fluid. The PCR method is particularly useful for the detection of asymptomatic HSV virus spread. 

The biggest limitation of the HSV NAATs amplification test is the cost of the test. Such special samples should be collected with a Dacron wiper and placed in the virus transfer culture medium.

NAATs can be stored for 72 hours at 4” C, and samples should be kept at - 20” C for long-term storage. These NAATs are four times more sensitive than the virus culture method for detecting herpes simplex virus.
Herpes Virus Structural Diagram

Serum antibody assay

The HSV serum test may be valuable in the following situations:
i.                  HSV virus culture is negative and has recurrent genital symptoms or atypical herpes symptoms
ii.               Clinical diagnosis of genital herpes without experimental diagnostic evidence
iii.            Insufficient specimen collection or poor delivery
iv.             Investigate asymptomatic patients (i.e. sexual partners of genital herpes).

What is HSV Prevention Principle?

Prevention should be based on cutting off the transmission route, try to avoid close contact with patients, avoid harmful factors stimulating the body, and actively exercise the body to improve the body's immunity. 

If pregnant women have HSV-2 infection during the perinatal birth canal, cesarean section can be performed to avoid neonatal infections.

Avoiding contact with patients or injecting specific antibodies into susceptible people can reduce the risk of HSV transmission.
Saliva, urethra or reproductive tract of asymptomatic people are important carriers of HSV-2. Sexual contact should be avoided if damage occurs. 

In some cases (such as when the amniotic membrane is not broken), a cesarean section can be taken to reduce the exposure of the newborn to the damaged genitals.
Injecting newborns with specific antibodies or gamma globulin after delivery can also be used as an emergency precaution.


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

About Me | Linkedin | Quora Profile | Medium Profile | Twitter

See Also:
  • Herpes Simplex Virus
  • Typhoid


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