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Cell-mediated immunity to herpes simplex virus envelope, capsid, excreted, and crude antigens was studied by in vitro lymphocyte stimulation tests during 198 recurrent attacks in 69 patients.
The clinical picture of herpes simplex virus type 2 (HSV-2) infection includes genital blisters and less frequently meningitis, and some individuals suffer from recurrent episodes of these manifestations. Herpes simplex virus type 1 (HSV-1) is a naturally neurotropic DNA virus proficient in establishing latent infection within neurons, but moreover possesses the ability to infect a wide range of celltissue types. Cell-mediated immunity against herpes simplex virus envelope, capsid, excreted, and crude antigens. Depressed specific cell-mediated immunity to Herpes simplex virus type 1 in patients with recurrent herpes labialis. The cytosolic factor ICP47 from herpes simplex virus (type 1 and 2) blocks peptide binding to TAP with nanomolar affinity and thus prevents peptide-stimulated ATP hydrolysis and peptide translocation into the ER lumen (1).
Cluster of Excellence Frankfurt (CEF) – Macromolecular Complexes, Goethe University Frankfurt, Frankfurt, Germany. If that's not what you want, the links at the top and to the left of this page may help you find what you're looking for, or something related to it.
Abstract Herpes simplex virus (HSV), a human pathogenic virus, has evolved several strategies to evade the production and function of interferons (IFNs) and cytokines generated by the innate immune system to restrict the virus. Creative Commons Attribution License (CC BY) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Herpes simplex virus 1 (HSV-1) infects the cornea and then establishes latency in sensory neurons of the trigeminal ganglia (TG).
We have a novel “humanized” HLA-A*0201 transgenic (HLA Tg) rabbit model of ocular HSV-1 that develops spontaneous reactivation, recurrent corneal disease and mounts specific CD8+ T-cell responses to human HSV epitopes.
Over the past 6 years, we have systematically determined that The HSV-1 Latency-Associated Transcript (LAT), the only viral gene that is abundantly transcribed during latency, increases reactivation. As literature on cell-mediated immune responses in patients with recurrent HSV-2 meningitis is lacking, we set forth to characterize immune responses in this disease with the aim to detect immune defects or deviations in patients with recurrent HSV-2 meningitis that may help to explain why some individuals get meningitis as a complication to viral reactivation. Despite existing humoral immunity, however, wild-type HSV is proficient in evading the immune system. The type I membrane glycoprotein US6 from human cytomegalovirus inhibits ATP binding to TAP via its ER-luminal domain, whereas peptide binding is not affected (2). After virus entry, the viral capsid is transported to the nucleus and the genome released into the nucleus through nuclear pores. Several countermeasures against the host IFN and proinflammatory response have been established by HSV. Equilibrium exists between the virus and the immune response, and a shift in this delicate balance either restricts the virus or enhances virus spread and tissue damage.


Sporadic spontaneous reactivation of HSV-1 causes shedding of virus in tears with no clinical disease (asymptomatic) leading to spread of virus to other individuals.
Although HLA Transgenic mice  can also mount humanized CD8+ T-cell responses, they do not develop recurrent corneal disease. One preparation consisted of HSV-1 nucleocapsid, and the other was a whole-cell lysate of HSV-2-infected cells, which includes nucleocapsid but also viral envelope antigens. The type I membrane protein UL49.5 from bovine herpesvirus uses a dual strategy to inhibit TAP function. Viral tegument proteins released into the cell support IE gene transcription or mediate takeover of the cell.
For instance, the IRF3 pathway is inhibited by ICP0, ICP27, and ICP34.5, through distinct mechanisms. Therefore, understanding of the cytokine response generated after HSV infection and the underlying virus-cell interactions is essential to improve our understanding of viral pathogenesis. Virus reactivation can also cause recurrent eye disease (symptomatic) and may lead to vision loss. This HLA Tg rabbit model will allow us for the first time to test the hypothesis that spontaneous HSV-1 shedding and recurrent eye disease can be reduced by “protective” CD8+ T-cell responses through therapeutic immunization with asymptomatic human CD8+ T-cell epitopes and a therapeutic strategy that interfere with the HSV-1 LAT immuno-evasion mechanism. Additional efforts are now focused on understanding how HSV-1 LAT regulates HSV-specific CD8+ T cell immunity within the TG following viral infection. Cell-mediated immunity to herpes simplex virus type 1 (HSV-1) was assessed by a lymphocytotoxicity 51-Cr-release microassay procedure, using the MA-160 human prostatic adenoma cell line chronically infected with HSV-1 and its parent cell line as control.
Cell-mediated immune responses to herpes simplex virus type 1 and type 2 virion and non-virion antigens were assessed in patients and in controls with oral leukoplakia, carcinoma and recurrent herpes labialis. Cell mediated immunity was studied by a cytopathic effect inhibition assay in mice infected in the ear with herpes simplex virus type 1 (HSV 1). First, it arrests TAP in a transport-incompetent conformation, while binding of peptide and ATP are unaffected (3). The IE proteins are mainly trans-activators that enhance the expression of E genes, which primarily encode enzymes involved in virus DNA replication. Also, the HSV L gene products ICP34.5 and Us11 inhibit PKR activation, with Us11 exerting its action by direct binding to dsRNA, for which reason Us11 potentially also blocks activation of TLR3 and RLRs. This review summarizes the current knowledge on induction and evasion of the innate immune response by HSV.
Validation of this hypothesis would have important implications for prevention of recurrent ocular disease. For instance we sought to determine if this impairment might involve LAT indirectly interfering with DC maturation.


Herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) are two of the eight known viruses which comprise the human herpesvirus family. Eventually, the L genes are expressed and new virus particles are assembled, matured, and released from the cell, either by cell lysis, endocytosis, or cell-cell fusion.
Work in The Laboratory of Cellular and Molecular Immunology (LCMI), at the University of California, Irvine has focused on understanding the molecular and cellular mechanisms used by HSV-1 to escape from the immune system. The subsequent reduced immunosurveillance by TG-resident CD8+ T cells may contribute to the known increased reactivation associated with LAT expression.
Animal studies suggest that activated macrophages, interferons, and, to a lesser extent, natural killer cells are important in limiting initial HSV infection, whereas humoral immunity and cell-mediated immunity are important in controlling both initial and recurrent infections. Herpes simplex viruses type 1 (HSV-1) and 2 (HSV-2) cause a variety of medically significant infections, especially in immunosuppressed subjects. Specifically, we are interested in evaluating how the herpes latency associated transcript (HSV-1 LAT), the only gene expressed during the latent phase, interferes with the immune cell functions.
Cell-mediated immune response to human immunodeficiency virus (HIV) type 1 in seronegative homosexual men with recent sexual exposure to HIV-1. In order to induce specific T cell-mediated immune responses, they act as the sentinels of the immune system and lie in wait in an immature state in almost all peripheral tissues (Banchereau & Steinman, 1998). The recently identified type II membrane protein CPXV12 from cowpox virus inhibits peptide translocation into the ER lumen by an as-yet-unknown mechanism (6). One major area of ongoing work in the laboratory is to study how HSV-1 LAT contributes to virus immune evasion from CD8+ T cells following mouse and rabbit ocular infection. HSV-specific CD8+ T cells are involved in protective immunity against ocular herpes, possibly through a combination of corneal and peripheral nervous system antiviral effects.
Herpes simples virus type 1 and 2 (HSV-1 and HSV- 2) and Varicella- zoster virus (VSV) are members of this subfamily.
Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) , also known as human herpesvirus 1 and 2 (HHV-1 and HHV-2) , are two members of the herpesvirus family, Herpesviridae, that infect humans. Viral epitope presentation with MHC class I is a requirement for activation of cytotoxic T-lymphocytes (CTLs) , the major effectors of the cell-mediated immune response against virally-infected cells.
The effect of daily valacyclovir suppression on herpes simplex virus type 2 viral shedding in HSV-2 seropositive subjects without a history of genital herpes.



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