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Latent, Recurrent Infection and Prevention of Herpes Simplex Virus


The herpesvirus family is a double-stranded DNA virus with an envelope structure. The length of the viral genomic DNA is about 120-240 kb. According to biological characteristics and genomic structure, the herpes virus family can be divided into three subfamilies: α, β and γ. Herpes simplex virus (HSV) is a subfamily of alpha, widely distributed in nature, can infect humans and many animals, especially human skin tissue has strong tropism.

Herpes virus mainly infects the host through skin, mucous membranes and nerve tissue to cause corresponding lesions, and is a common pathogen of human viral diseases. Herpes simplex virus can be divided into two serotypes, HSV-1 and HSV-2. HSV-1 mainly causes cold sores, pharyngitis and keratitis after infection in human body, and can also cause serious diseases such as sporadic encephalitis; HSV-2 Mainly caused by damaged skin and mucosal infections genitalherpes, GH. Epidemiological investigations in recent years have found that HSV-1 and HSV-2 occupy an equally important role in the pathogen causing genital herpes virus, and can be lurking in the body for a long time. During the latent infection process, the structure and function of the herpesvirus genome were not affected or destroyed, and a series of regulation related to viral gene transcription and expression were in a state of stagnation. There is no complete genomic replication in this process, but there is limited local gene transcription and entry into the proliferative replication phase under specific conditions. The proliferative replication of herpes simplex virus is a series of transcriptional events caused by the interaction between the virus’s own regulatory proteins and specific molecules in the cell, but it is known about the process of transcriptional regulation of viral genes in latent states and its process of replicating proliferation. less. At present, the incidence of genital herpes is rapidly increasing and it is easy to relapse, which has caused great difficulties in the treatment and prevention of related diseases. To elucidate the related mechanisms of latent infection and recurrence of viruses, it is important to further reveal the nature of recurrence of HSV infection and establish therapeutic targets to effectively prevent and treat HSV infection and late recurrence. This article reviews the biological characteristics of herpes simplex virus, possible latent recurrence mechanisms, clinical prevention strategies for HSV infection, and recent advances in the development of HSV vaccines.


  1. Biological characteristics of herpes simplex virus

HSV-1 consists of a globular virus composed of a capsule, a capsid, a core and a capsule. The core of the virus is double-stranded linear DNA, and the filament reel is wound, about 125-240 kb. The genome of HSV-2 is approximately 154 kb. The genome of HSV-2HG52 strain has a G + C content of about 70%, consisting of a 18% short fragment (S) and a 82% long fragment (L) covalently linked by the L-S junction. Each fragment includes inverted repeats (TRL, IRL, IRS, and TRS) at both ends and a unique sequence (ML and US) in between. Due to their different linkages, the HSV-2 gene has four isomer molecules. The transcriptional regulation mechanism of HSV is diverse, the genome structure is complex, and the number of genes is large and overlapping.

The HSV-2 gene is transcribed and expressed through strict cascade regulation, and is classified into immedi-ate-early gene, IE or α, early gene, E or β, late gene, L or γ according to chronological order. The immediate early gene is the first expression after infection and can be transactivated by the late viral protein VP16. The activation and replication of the latent infection of the virus are closely related to the immediate early protein or infected cell polypeptide, ICP, including ICP47, ICP4, ICP27, ICP22 and ICP0. ICP0 and ICP4 play the most important role in viral replication. The replication of early genes regulates the transcriptional expression of early and late genes by inducing the trans-acting of proteins encoded by immediate early genes while cascading. The early genes are β1 and β2, and β1 is composed of ICP6 and ICP8. β2 is the main viral protein of viral nucleic acid metabolism, including thymidine kinase and DNA polymerase. The products of late genes are mainly structural proteins of viruses, including some glycoproteins, capsid proteins and intimal proteins, which are involved in the adsorption, entry and fusion of viruses and the antigenicity of viruses.


  1. Latent infection mechanism of herpes simplex virus

HSV is highly contagious and can cause a wide range of prevalent diseases and is easy to establish latent infections. HSV-1 and HSV-2 can be lurking in the trigeminal ganglion and the appendix ganglion, respectively. Kesan et al. have defined the latency of HSV-1 as follows:①The virus can persist in the host but the host itself does not exhibit any relevant clinical symptoms;②The latently infected HSV virus can be reactivated by the latent state and produced with infectious virus particles;③When the virus is in a latent infection state, it does not express any related proliferative genes, but a large amount of La-tency-Associated transcripts, LATs are accumulated in the host cell nucleus;④The virus does not express the relevant antigen, but the presence of the viral genome can be detected in the host.This definition defines the phenotype of HSV-1 latent infection from four different levels and is consistent with HSV-2 latent infection. Although with the gradual development of detection technology, viral proliferative infection genes such as ICP0 and TK kinase are also slightly expressed during latent infection of the virus, but the researchers believe that this is caused by the dynamic balance between latent infection and reactivated infection. The main causes of latent infection in HSV-2 virus are as follows: 1 immune escape after viral infection; 2 inhibition and regulation of immediate early protein expression by the virus; 3 interaction between viral genome and host cells, including Viral gene inhibition of cellular protein, RNA synthesis, selective translation of HSV-infected viral mRNA, regulation of herpesvirus on cell cycle system and apoptosis, etc.; 4 viral genome-encoded microRNA-mediated regulation; 5CTCF passage The sequence specifically bound by CTCF on the HSV genome regulates its late recurrence.

2.1 HSV evades immune surveillance mechanisms DNA and RNA viruses from different species may evade surveillance by the immune system and persist in the host for long periods of time. Successful immune escape of the virus is one of the leading causes of chronic herpes virus infection. Its mechanism mainly includes the following six aspects.

2.1.1 Restrictive expression of viral genes

Almost all viruses use this method to different extents to avoid surveillance of the host immune system, and herpes virus and some retroviruses are particularly prominent. Once the herpes simplex virus is latent in the neurons, all of the genes in the viral gene organization, except one, stop transcription, leaving almost no trace of the virus in the infected neurons. Numerous studies have shown that LAT has a function of inhibiting viral gene expression.

2.1.2 Use the immune exemption portion of the host

A small number of tissues and organs of the human body are parts that immune cells are not allowed to intervene, and enjoy the “privilege” of immune immunity. Therefore, viruses entering the immune-immunized site can temporarily avoid the surveillance of the immune system without causing local inflammatory reaction. The blood-cerebrospinal fluid barrier of CNS limits lymphocytes from entering the CNS and is therefore less susceptible to recognition by T lymphocytes. Therefore, the CNS is a long-term chronic infection and latent organ of several viruses including HSV.

2.1.3 Variant HSV viruses of viral antigens can also evade host immune surveillance through genetic mutations.

The antigen encoded by the viral gene is also mutated. Variation of surface antigen may cause the virus mutant to temporarily avoid the neutralization or conditioning effect of the existing antibody, and obtain a certain survival advantage. CTL and Th cells play an important role in the complete elimination and control of chronic infection of the virus, which recognize T lymphocyte epitopes in viral protein molecules presented by MHC molecules. If the gene mutation in the in vivo reproduction of the virus just changes the original T lymphocyte epitope, the new peptide can no longer bind to the host’s MHC molecule, or it can not be recognized by T lymphocytes. The virus mutant can temporarily avoid the effects of CTL and Th cells, and obtain the reproductive advantage that the parent strain does not have. This phenomenon has been confirmed in HSV, hepatitis B virus and Epstein-Barr virus.

2.1.4 Interfering with host cell antigen presentation

Lipid antigens presented by CD1d molecules on the surface of antigen-presenting cells can induce NK cell immune responses, which is very important for host defense against viral antigens. Liu et al found that HSV-1 infection can inhibit the expression of CD1d molecules on the surface of antigen-presenting cells. This is not because HSV inhibits the synthesis of CD1d, but because it redistributes the endocytosed CD1d molecule to the lysosomal membrane, thereby preventing the endocytosed CD1d molecule from reappearing on the cell surface. It may also be because HSV inhibits the transport of newly synthesized CD1d molecules to the cell surface. Studies have also shown that HSV-encoded ICP47 binds to the antigen-presenting-related carrier TAP-1/2, prevents viral proteins from being transported to the endoplasmic reticulum, is loaded onto the nascent MHC-I molecule, and is ultimately presented to CD8+ T cells.

2.1.5 Inhibition of TCR signaling T lymphocytes is an important component of the immune response against HSV infection.

Yang et al. found that HSV inactivates T cells by inhibiting TCR signaling. Inhibition of TCR signaling occurs both at the T cell activation junction of the TCR signaling cascade and at the step away from the T cell activation junction, including for calcium flux and multiple MAPK (mitogen activated protein kinase) ) inhibition. HSV-induced T cell inactivation results in decreased levels of T cell activation linker phosphorylation at tyrosine residues, whereas phosphorylation of tyrosine residues is important for TCR signaling.

2.1.6 Interfering with the function of immune effectors

Interferons are at the forefront of host resistance to viral infection, and numerous studies have shown that interferon is a family of soluble proteins that mediate the host’s antiviral effects, regulating cell growth and activation of immune responses. The inherent antiviral activity of interferon is very efficient and fast. Therefore, many viruses evade host immune surveillance by inhibiting the synthesis of interferons or downstream antiviral effects. Davis et al. found that HSV-encoded ICP34.5 plays an important role in evading the innate immune response of the host. ICP34.5 dephosphorylates eIF2α, a translation initiation factor phosphorylated by PKR in an antiviral response, thereby reducing the expression of cytokines such as interferon-β. The Mogensen study found that HSV-1 promotes viral gene expression of the laminin VP16 by inhibiting the expression of pro-inflammatory cytokines by reducing the stability of IL-6 mRNA. This inhibition is not directly mediated by VP16, but relies on ICP4 (infected cellular protein) and ICP27, which are encoded by the immediate early gene of the virus. In the early stages of HSV infection, they are expressed in a VP16-dependent manner. The HSV envelope glycoprotein gC is capable of binding to complement C3b, so that the virus is not neutralized by the complement component. Experiments have shown that wild HSV strains also maintain complete invasiveness in the presence of complement, whereas mutants that do not express gC are neutralized by complement even in the absence of antibodies.

2.2 The role of LAT gene in latent recurrence of HSV

The LATs family includes major LATs (composed of 2.0 kb, 1.5 kb, 1.45 kb) and non-primary LAT (composed of 8.3 kb). These RNA moieties are linear and partially annular, but are activated by different folding methods. The non-primary LAT is an 8.3 kb transcript that is spliced to obtain a 2.0 kb LAT, and then cut about 500 bp to generate a 1.5 kb or 1.45 kb LAT. LAT is believed to play an important role in the efficient establishment of latency. It was also found that the deletion of a small fragment of the partial sequence of the LAT promoter resulted in a sharp decrease in the number of latently infected cells, thus revealing that transcription of LATs is the key to establishing latent infection. LAT is versatile and plays a role in the establishment and maintenance of HSV latency. At present, the strategy of deletion mutation is mainly used to study the role of LAT in latent infection.

2.2.1 The role of LAT in establishing latent infections

LAT is thought to play an important role in the efficient establishment of latent processes. The deletion of small fragments of the LAT promoter sequence can lead to a sudden decrease in the number of latently infected cells, suggesting that LAT transcription is the key to establishing latent infection.

2.2.2 The role of LAT in maintaining latent infection

The maintenance mechanism of HSV virus latency is still unclear. There are two hypotheses of antisense transcriptional repression mechanisms. One hypothesis is that 2.0kb LAT inhibits the expression of ICP0 protein and blocks viral replication through the antisense RNA mechanism during latency; another hypothesis is that non-primary LAT is in the latent process. The antisense RNA mechanism is used to inhibit the expression of ICP4 protein, thereby preventing the replication of the virus and delaying the entry of the virus into the lysis phase. Studies have found that there are several groups of mRNAs transcribed from lytic viral genes during latency, which are difficult to detect due to low levels of transcription. In the latent process of LAT mutant virus strain, Chen et al. detected that the transcript expression level of the immediate early protein ICP4 gene and the early protein TK gene was several times higher than that of the wild virus. Further studies revealed that ICP4 down-regulates the expression of the RNA-binding protein-rich G-sequence factor (GRSF1) by binding to the precursor of miR-101, hsa-mir-101-2, and inhibits the replication of HSV-1 virus.

2.2.3 The role of LAT in viral recurrence

The expression of early LAT genes during relapse may play an important role in promoting lytic genes from silencing to expression. During the latent process, ICP4 mRNA is always expressed in the ganglion, albeit at a very low expression level. Therefore, when the ICP0 mRNA appears and its expression level is up-regulated, it can be used as a marker for the virus to enter the cleavage replication phase. Experiments have shown that in the LAT gene mice, the amount of HSV-1 virus DNA is three times that of LAT-deficient mice, and its activation and expression are related to CD8, PD-1 and Tim-3.

2.2.4 LAT performs anti-apoptotic function by encoding microRNA

MicroRNAs (miRNAs) are a new class of small-molecule single-stranded non-coding RNAs that regulate gene expression and are important factors in the regulation of RNA stability and translation efficiency in animals, plants and viruses. Both HSV-1 and HSV-2 LATS encode multiple functional miRNAs, and their expression in latency is much higher than during acute infection. For HSV-1, CUI, etc., through computer simulation and alignment with miRNAs, 24 pairs of candidate miRNAs and 13 pairs of miRNA precursors were found. In 2010, Igor Jura et al. confirmed 17 miRNAs expressed by HSV-2 by high-throughput sequencing. So far, there are 18 kinds of miRNA libraries MiRBase. Our recent study confirmed that miR-H4-5p encoded by HSV-2LATs can target CDKN2A and CDKL2 genes in infected host cells, causing a decrease in mRNA and protein levels and anti-ActD-induced apoptosis. The effect can also promote the cell cycle into the S phase and promote cell proliferation. However, miR-H3 can exert anti-ActD-induced apoptosis, but has no obvious effect on cell cycle, and its specific molecular mechanism is still not fully understood. This indicates that the HSV-2 miRNA regulates the expression of the virus itself and the host gene, exerts an RNA interference effect, thereby inhibiting neuronal apoptosis, and is beneficial for maintaining the virus to continue to be latently infected. By up-regulating or down-regulating miRNA expression, the expression of the gene of interest can be altered to achieve therapeutic or interventional goals. As a new class of drug targets, miRNAs have received increasing attention. The new idea of ​​HSV-2 treatment will start from miRNAs to specifically prevent or destroy HSV-2. Although these are still in the experimental stage, there are reasons to believe that small molecule miRNA drugs are also expected to become a new method for the treatment of latent infection of HSV.

2.3 The role of CTCF in the latent recurrence of HSV

CTCF contains 727 amino acid residues, and the middle segment (M segment) has 312 residues forming 11 consecutive zinc finger structures. The amino terminus (N segment) and the shuttle end (C segment) have 265 and 150 residues, respectively. A widely expressed and highly conserved 11 zinc finger DNA binding protein that binds to a DNA target site of approximately 50 bp in length by zinc fingers to form different CTCF-DNA complexes, which can be regulated by targets on different genes. Functions, including gene silencing by transcriptional repression and activator regulation, methylation-dependent chromatin insulation, and eukaryotic histone acetylation, parental imprinting, and heterochromatinization of chromosomes play an important role and are formed by themselves. Multimers or interact with other proteins and colocalize with subcellular nuclear structures, participate in the formation and maintenance of specific chromatin structures and play a key role in epigenetic regulation. CTCF is the central link of regulatory networks related to cell growth, proliferation and phylogeny. There is a significant correlation between CTCF mRNA decline, protein decline and cell growth inhibition, suggesting the importance of normal CTCF expression for cell growth. . Many insulator sequences have many CTCF binding sites on which methylation of DNA prevents the binding of CTCF and inhibits the function of CTCF. CTCF is also the only transcription factor that has been experimentally demonstrated to mediate the blocking function of different insulator enhancers. CTCF is the core protein of the high-level structure of tissue chromatin. Its function from Drosophila to humans, including some human pathogens such as EBV, KSHV and HSV, is very conserved and can cause epigenetic changes, using pattern viruses. Study the law of chromatin’s high-level structure on external invasion.

Studies have shown that there are many CTCF-specific sequences on the HSV-1 genome, especially in the LAT, ICP0 and ICP4 regions. During HSV-1 latent infection, the insulator is enriched with CTCF protein, and wild-type latent HSV-1 is accompanied by CTCF detachment from its binding sequence under activation stimulation. The CTCF binding sequences upstream of ICP0 and ICP4 are typical insulators that attenuate the effects of the LAT enhancer. In general, during the latent and activating process, the degree of binding of CTCF to its binding sequence is regulated according to different stages, thereby affecting the expression of HSV-1 gene. Therefore, epigenetic regulation plays a very important role in the conversion process of HSV-1 latency and reactivation. The HSV-1LAT 2.0 kb intron has a large number of CTCF binding sites, and CTCF can regulate the expression of genes involved in viral replication by binding to and detachment from these sites, thereby affecting the latent and relapse of the virus. The latest research of this research group is for the first time to explore the combination of CTCF on HSV-2. It is found that the CTCF binding site exists in the 3′ end of HSV-2 LAT and intron, which has the effect of weakening the function of gene promoter. May play a key role in the latency of HSV-2. It has found a new direction for the study of HSV-2 latent recurrence mechanism and treatment ideas.


  1. Progress in prevention and treatment of HSV infection

3.1 Clinical treatment of HSV infection The current treatment targets for HSV infection mainly include alleviating symptoms, reducing recurrence, reducing detoxification and reducing the psychological burden of patients. The main treatment methods include systemic antiviral therapy, local treatment, immunotherapy and health education. Referring to the recommendations of the 2009 Chinese genital herpes clinical diagnosis and treatment guidelines, systemic antiviral is currently the most important treatment, commonly used drugs are acyclovir, valaciclovir and famciclovir, divided into intermittent therapy and long-term inhibition therapy . Intermittent therapy is the time of onset. It is recommended to give antiviral drugs within 24 hours after the patient has prodromal symptoms or skin lesions: oral acyclovir 200mg 5 times / d for 5d; or acyclovir 400mg 3 times / d, a total of 5d; or valacyclovir 500mg twice / d, a total of 5d; or valacyclovir 300mg 2 times / d, a total of 7d; or famciclovir 250mg 3 times / d, a total of 5d. Among them, antiviral treatment for initial herpes simplex, the course of treatment needs to be extended to 10 days. For patients with frequent episodes (more than 6 episodes per year), long-term inhibition therapy may be recommended: oral acyclovir 400 mg twice daily/d; or valacyclovir 500 mg once daily, usually for 6 months or longer time. Although long-term inhibition therapy can reduce the number of recurrences of herpes simplex, there is no evidence that this method can prevent recurrence after stopping the drug. In addition, the local treatment of herpes simplex has certain auxiliary effects, including the use of physiological saline, 3% boric acid solution, etc., or wet dressing, no obvious exudation, topical 3% acyclovir cream, 1% spray Ciclovir cream and so on. Combined application of immunotherapy is also an important method for the treatment of herpes simplex in clinic. Commonly used immunomodulators include thymosin, interferon, transfer factor, IL-2, levamisole and imiquimod. Taking necessary health education and psychological interventions for patients to educate them to maintain regular lifestyle habits, proper physical exercise and good mental state are just as important as medication.

3.2 Progress in prevention and vaccine development of HSV infection

3.2.1 Prevention of HSV infection

Antiviral therapy or combined immunotherapy, it is difficult to completely eliminate HSV in the body to achieve a healing effect, so the prevention of HSV infection is particularly important. Counseling, sex education and vaccination are the most important preventive measures. Herpes simplex infections include patients with current disease, subclinical or asymptomatic detoxification patients, which are more clinically important because the latter two are more concealed. Avoid unsafe sex, use condoms throughout, and timely treatment of sexual partners is the most basic preventive measure. Developing efficient and safe vaccines is the key to preventing and treating HSV infection.

3.2.2 HSV vaccine research HSV vaccine research has been carried out for many years, and has made some progress, but the current vaccine research for HSV is still in the in vitro experiment, animal experiment and pre-marketing clinical trial stage, and there is no approved HSV vaccine on the market worldwide. According to the composition and mechanism of action, HSV-2 vaccine can be divided into inactivated vaccine, live attenuated vaccine, replication-deficient virus vaccine, subunit vaccine, peptide vaccine, live vector vaccine and DNA vaccine. The previously developed HSV inactivated vaccine has been discontinued due to its poor efficacy, low immunogenicity and potential carcinogenicity. Live attenuated vaccine

The live attenuated vaccine is a gene-killing method to delete genes related to HSV virulence, latent or revived functions, and obtain an attenuated vaccine strain which has replication ability and immunogenicity but has no pathogenicity or low pathogenicity. . At the beginning of 2000, several live attenuated HSV-2 vaccine trials showed that the vaccine prevented 37.5% of patients from recurring. Recently, the development of HSV-2 ICP0-mutant vaccine strain has progressed. The HSV-20ΔNLS vaccine strain has been confirmed by animal experiments to have good safety and immunogenicity. It is reported that 115 mice were inoculated with HSV-20ΔNLS strain. 114 patients survived the HSV virus challenge, while 45 mice in the control group were vaccinated with the gD subunit vaccine, and only 3 survived the virus challenge, demonstrating a 10-100-fold potency over the gD subunit vaccine, indicating This is a strong candidate for HSV-2 vaccine. Another attractive candidate for live attenuated HSV-2 vaccine is HSV-2-gD27. In vitro and animal experiments have confirmed its loss of appeal to neuronal cell lines and sensory ganglia in mice, and immunogens can be produced after vaccination. Loss of pathogenicity. The main drawback of the application of live attenuated vaccines is that it may produce wild-type HSV. Replication defective virus vaccine

The replication-defective virus vaccine is a special type of live vaccine that removes essential genes for partial viral replication, and also demonstrates its good safety and immunogenicity. The non-infectious single-cycle virus (DISC) developed in 2000 is a special replication-defective HSV mutant. By deleting the UL22 gene region, the virus cannot encode gH glycoprotein and cannot infect normal cells. The results are not ideal, although it has good safety, it can not effectively control the recurrent infection of HSV-2 and improve the course of disease. The main candidate strains of replication-deficient virus vaccines currently under investigation include ACAM529, CJ2-gD2 and gE2-del strains. Subunit vaccine

Subunit vaccines are the most studied type of HSV vaccines, which are prepared by combining recombinantly expressed HSV subunit components as antigens with appropriate adjuvants. The surface glycoprotein of the virus is usually used as an antigen such as gD and gB. The gD2-aluminum-MPL vaccine was developed by GSK. After two phase III clinical observations, the vaccine was only effective in women who were negative for HSV-1, but not for women who were seropositive for HSV-1 and all men. Significant protection. The latest large randomized, double-blind clinical trial involving 8323 women confirmed that the vaccine is effective in preventing HSV-1 infection, but does not prevent genital herpes and other infections caused by HSV-2 infection. The results of these studies suggest that a simple glycoprotein or several glycoproteins may not be able to induce an immune response to HSV-2. However, some new potential subunit vaccines such as: gD2ΔTMR340-363 (ICP4383-766), gD-Fc, gC2&gD2, etc. are under development, which brings new hope for the development of effective HSV-2 vaccine. Peptide vaccine

The synthetic peptide contained in the peptide vaccine can induce a protective immune response against HSV, which can act on T cell or B cell epitopes in vivo. Recent animal and human experiments have shown that peptide vaccine has good immunogenicity. It can induce HSV-specific CD4+ and CD8+ T cell responses in vivo, and peptide vaccine is also one of the potential candidate vaccines. Live vector vaccine

A live vector vaccine is a heterologous vector (eg, adenovirus and vaccinia virus) that expresses certain subunit components of HSV, and inoculation of the host elicits a strong HSV-specific immune response. Studies have shown that the vaccinia virus Ankara (MVA) vector expressing HSV-2 gD induces strong cellular and humoral immunity. In addition, recombinant V. cholerae vectors (rVCG) expressing Chlamydia MOMP and HSV-2 gD induced high levels of expression of Chlamydia and HSV-2 antibodies in vivo and elicited a strong Th1 immune response. The main disadvantage of such vaccines is that the presence of heterologous vectors may trigger different expression of antibodies in humans, affecting the efficacy of vaccines, and may also pose a threat to human health. DNA vaccine

The DNA vaccine originated in 1990 and is a new idea for the development of HSV vaccine. Since the gD2 and gB2 genes are the main antigens that induce immune responses and are widely used to construct HSV DNA vaccines, a clinical study of HSV-2 DNA vaccines has demonstrated that it can induce specific cellular immune responses without inducing humoral immunity. . It can be seen that the immune effect of DNA vaccine needs to be further improved.


  1. Conclusion

As the understanding of herpes simplex virus continues to increase, people will re-understand the mechanisms by which HSV establishes latent and adaptive immune systems that lurk and evade the host. New ideas for HSV treatment will target or prevent HSV from miRNAs. Although these are still in the experimental stage, there is reason to believe that through the efforts of researchers, it is possible to develop drugs that completely cure the diseases caused by HSV. At present, there are still many problems to be solved in the development of HSV vaccine, and it may take time to finally come out. A more in-depth study of the immunological characteristics and infection mechanism of HSV will have important guiding significance for the development of vaccines.

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