Studies conflict as to whether or not the Herpes virus affects your entire immune system. ), 3Department of Biotechnology, Graduate School of Engineering, Osaka University, Suita City, Osaka 565-0871, Japan; moc.liamg@mcobgunono. Recently, Liu et al. Herpes virus and autophagy: All right, everybody be cool, this is a robbery!. Schenkel J.M., Masopust D. Tissue-resident memory T cells. The authors had earlier shown that COR-1 induces a balanced adaptive humoral and cell-mediated immune response in mice, and protected mice challenged with a lethal dose of HSV-2 [142], and was also shown to elicit minimal adverse effects when tried in healthy volunteers [116]. Wang H, Davido DJ, Mostafa HH, Morrison LA. The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). It has also been demonstrated that exogenous p62/SQSTMI decreased the HSV viral yield [52], thus confirming a potent antiviral activity, but the exact mechanisms by which the proteins mount antiviral responses still needs to be elucidated. Ranjbar Z, Lavaee F, Karandish M, Peiravian F, Zarei F. BMC Oral Health. Herpes simplex virus genes, Us3, Us5, and Us12 differentially regulate cytotoxic T lymphocyte -induced cytotoxicity. It was reported that the candidate vaccine stimulated both humoral and cellular immune responses while exhibiting minimal adverse effects in the HSV-2 seropositive persons with genital herpes [4]. Immune System Okonko I.O., Cookey T.I. A single intramuscular vaccination of mice with the HSV-1 VC2 virus with mutations in the glycoprotein k and the membrane protein UL20 confers full protection against lethal intravaginal challenge with virulent HSV-1 and HSV-2 strains. Accessibility The 134.5 protein of HSV-1 was said to inactivate STING and, more so, disrupts its translocation from endoplasmic reticulum to golgi apparatus, an important process necessary to prime cellular immunity [87]. ); ude.enyaw@razaele.drawer (E.E.R. [Herpes simplex virus vaccine studies: from past to present]. WebYes. And even in healthy people, there are rare instances where HSV-1 can spontaneously cause inflammation of the brain, resulting in irreversible brain damage. In other words, herpesviruses prevent alarming our cells about the infection, allowing the virus to spread in our system and hide from our immune system. Herpes simplex virus (HSV) infections are among the most common viral infections and usually last for a lifetime. Two, it makes the transporter stuck in this conformation.". WebMayo Clinic Minute: How to maintain a healthy immune system. The existing challenges related to the deployment of a HSV vaccine in humans include the expensive costs of carrying out trials to test the efficacy of HSV vaccine candidates, and this is especially critical, as most of the candidates that exhibited potency in animal models did not confer same protection in humans [155]. Is the ketogenic diet right for autoimmune conditions? Can You Die from Herpes? Know the Risks of the Different Types If you happen to be experiencing anything out of the ordinary in your body, you should go to a healthcare expert nearest to you and relay any concerns that you may have. Yu W., Geng S., Suo Y., Wei X., Cai Q., Wu B., Zhou X., Shi Y., Wang B. We've got the parenting tips and information you need to raise a happy, healthy family. Wald A., Koelle D.M., Fife K., Warren T., Leclair K., Chicz R.M., Monks S., Levey D.L., Musselli C., Srivastava P.K. To create the workhorses or proteins, cells make working copies of the genes in the DNA that are relevant to them. Zheng C., Su C. Herpes simplex virus 1 infection dampens the immediate early antiviral innate immunity signaling from peroxisomes by tegument protein VP16. What COVID vaccine side effects can Us3, which is a serine/threonine kinase, inhibits Bad-induced apoptosis, while Us5 is a glycosylated J protein that inhibits Fas-mediated apoptosis [50]. Felsburg P.J. The virus outsmarts the immune system by interfering with the process that normally allows immune cells to recognize and destroy foreign invaders. "This work illustrates a striking example of how a persistent virus evades the immune system," says Chen. HSV-1 also inhibits autophagy through the protein Us11 [54]. The interferon-induced protein with tetratricopeptide repeat 3 (IFIT3) is an antiviral host intrinsic factor that restricts replication of DNA and RNA viruses. The association between ICP0 and PML-NBs is said to be a series of process involving adhesion, fusion and retention [72]. Herpezine is a specially formulated all-natural mixture of ingredients proven to help relieve and prevent HSV2 outbreaks when used as directed. . Chandra J., Woo W.P., Dutton J.L., Xu Y., Li B., Kinrade S., Druce J., Finlayson N., Griffin P., Laing K.J., et al. The structural component involves the skin and the mucus membrane. However, HSV-1 134.5 protein (late gene encoded) represses NF-B activation in CD8+ dendritic cells [22]. UL42 and HSV-1 34.5 protein inhibits the translocation of p50 and p65 subunits of NF-B by inhibiting the transcription of genes involved in inflammatory response. A Herpes Simplex Virus 2 (HSV-2) gD Mutant Impaired for Neural Tropism Is Superior to an HSV-2 gD Subunit Vaccine To Protect Animals from Challenge with HSV-2. doi: 10.1016/j.vaccine.2019.05.009. WebHerpes does not weaken the immune system. Primary immunodeficiency disorders also called primary immune disorders or primary immunodeficiency weaken the immune Another novel autophagy inhibition mechanism employed by HSV is the downregulation of the mitophagy [51], adaptor optineurin (OPTIN) and the autophagy adaptor protein sequestosome (p62/SQSTM1) [52]. One of the recent findings was on a study that focused on the Herpes simplex encephalitis and the impact of the bloodbrain barrier in modulating the pathological development of the disease [79]. The evasion of HSV-1-specific CD8+ T cells which accumulates in infection sites is enhanced by HSV-1 UL13 kinase through reducing the expression of the CD8+ T cell attractant chemokine CXCL9 in the CNS of infected mice, leading to increased HSV-1 mortality due to encephalitis [90]. Mundle S.T., Hernandez H., Hamberger J., Catalan J., Zhou C., Stegalkina S., Tiffany A., Kleanthous H., Delagrave S., Anderson S.F. National Library of Medicine Safety and immunogenicity of long HSV-2 peptides complexed with rhHsc70 in HSV-2 seropositive persons. Accidentally interfering with TAP or other similar transporters in an unintended way would likely disrupt many cellular processes and cause major side effects. The same authors reported that STING also activates the Jun N-terminal protein kinase/stress-activated protein kinase (JUN/SAPK) pathway. Glob. Vaccines for herpes simplex: Recent progress driven by viral and adjuvant immunology. It is not intended to provide medical or other professional advice. Bethesda, MD 20894, Web Policies Manipulation of host cell death pathways by herpes simplex virus. Zheng Y., Gu H. Identification of three redundant segments responsible for herpes simplex virus ICP0 to fuse with ND10 nuclear bodies. Xiong R., Rao P., Kim S., Li M., Wen X., Yuan W. Herpes simplex virus 1 US3 phosphorylates cellular KIF3A to downregulate CD1d expression. The histone chaperon HIRA promotes the induction of host innate immune defenses in response to HSV-1 infection. Hu M.M., Yang Q., Xie X.Q., Liao C.Y., Lin H., Liu T.T., Yin L., Shu H.B. ; supervision, A.C.I. Micro-RNA-155 (miR-155) was reported to contribute to the pathogenesis of stomal keratitis [100]. This positive outcome of COR-1 in HSV-2 positive patients lends credence to the potential of COR-1 as a HSV therapeutic vaccine. This article will hopefully shed some light and answer the question: does herpes weaken your immune system? Inclusion in an NLM database does not imply endorsement of, or agreement with, This is normally attributed to the high latency potential of the virus. J Virol. The mucus membrane is less impermeable compared to the skin. van Wagoner N., Fife K., Leone P.A., Bernstein D.I., Warren T., Panther L., Novak R.M., Beigi R., Kriesel J., Tyring S., et al. The https:// ensures that you are connecting to the Researchers from the University of Cambridge in the UK, and two German institutions: the Julius-Maximilians- Universitt Wrzburg and the Ludwig-Maximilians-Universitt Mnchen, report their findings in the journal Nature Communications. This stabilizes the sample, allowing scientists to retrieve data and computationally determine the structure. Now and again, the virus flares up and causes mild cold sore symptoms. Lahmidi S., Strunk U., Smiley J.R., Pearson A., Duplay P. Herpes simplex virus 1 infection of T cells causes VP11/12-dependent phosphorylation and degradation of the cellular protein Dok-2. WebThe Interplay of Herpes Simplex Infection and the Immune System The hostpathogen interaction is dynamic that has the potential to result in a diseased condition. However, understanding the various ways viruses block transporters could be harnessed for treating other diseases. Horng T., Barton G.M., Flavell R.A., Medzhitov R. The adaptor molecule TIRAP provides signalling specificity for Toll-like receptors. ICP0 promotes viral replication and reactivation from latency by inhibiting interferon synthesis [16]. Sci. Herpes simplex virus belongs to the Herpesviridae family, a group of spherical viruses measuring 120200 nm. Disclaimer. Geltz J.J., Gershburg E., Halford W.P. Role of miRNA-155 in the pathogenesis of herpetic stromal keratitis. CD4+CD25+ T cells regulate virus-specific primary and memory CD8+ T cell responses. Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a healthcare professional. CD4+ CD25+ has reportedly been involved in HSV-1 response [30], and the deletion of CD4+ cells increased susceptibility to HSV-1 infection in mice [31]. The initial response is due to whats called the innate immune response . It's a transporter that acts as a bridge to move the virus pieces across the membrane of the endoplasmic reticulum, a structure within the cell that packages the virus bits. Another group in their study explored the possibility of maternal immunization with the single-cycle HSV candidate vaccine deleted in glycoprotein-D [148,149,150], which induces antibody-dependent cell-mediated cytotoxicity (ADCC) to confer protection to neonates. Careers. It has been reported that HSV-1 downregulates CD1d cell surface expression and suppresses the function of NKT cells through its viral protein kinase US3 [92]. It has been shown that HSV-1 not only inhibits autophagy in neuronal cells, but also in non-neuronal cells. Pathog. WebDoctors & departments. Critical role of regulatory T Cells in the latency and stress-induced reactivation of HSV-1. Two distinct features of the adaptive immune system are specificity and memory. The immune system which consists of an innate and adaptive component has cytosolic sensors which sense the DNA of this virus and consequently stimulate inflammatory response against it. It is also possible to acquire herpes through direct contact on the eyes but never through physical contact with an object or a surface. They note this is an ideal cell for investigating how HSV-1 seizes control of RNA molecules and gene transcription. As a professional writer at many renowned websites. Furthermore, pathogen pattern receptors such as the toll-like receptors (TLR) and nucleotide-like oligomerization domain like (NOD-like) receptors play vital roles in innate immunity. Working first with a mouse model, and then repeating the results in humans, the team found that after initial infection, the host protein interferon gamma kept the virus dormant in the body. They survive by inserting their DNA into the DNA of host cells so that instead of making proteins for the cells, the cell machinery makes virus proteins and copies of the virus. UL41: Virion host shutoff (Vhs); cGAMP: Cyclic guanosine monophosphate (GMP), Adenosine monophosphate (AMP); cGAS mRNA: Cyclic GAMP synthase messenger ribonucleic acid; ICP: Infected cell protein; TBK1: TANK-binding kinase 1; STING: Stimulator of interferon genes; NF-kB: Nuclear factor kappa B; IRF: Interferon regulatory factor 3. Vaccine. Promyelocytic leukaemia nuclear bodies (PML-NBs), also referred to as nuclear domains 10 (ND10), or PML oncogenic domains (PODs), are small (0.11.0 m) dynamic nuclear structures made of several constant (PML, SP100, Daxx) or transiently associated proteins, depending on the cell function and/or exposed stress [60,61,62]. Moreover, ICP0 utilizes different motifs of PML-NBs fusion and SUMO interaction [72], suggesting different molecular mechanisms of PML- ICP0 interaction and degradation. A study investigated the role of LAT encoded miRNAs in resistance to apoptosis and establishment of latent infection [97]. A PYRIN protein interferon gamma inducible protein 16 (IFI16), which functions as a cytosolic DNA sensor that directly binds DNA, has been reported. University of Cambridge , accessed 25 May 2015. With that being said, again, it is not that easy to just say that herpes boosts or weakens our immune system. IFI16 is an innate immune sensor for intracellular DNA. herpes simplex virus; immune response; immune system; vaccine. Cold Hands 2. 2023 Healthline Media UK Ltd, Brighton, UK. The same authors also found out that the overexpressing of two proteins KIF1B and KIF2A, which are both members of the kinesin-3 family [48], attenuated this rate of egress via reduced lamin degradation. Accessibility Bacterial vs. Our findings provide a mechanistic explanation for how it's able to escape detection by immune cells.". This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (, herpes simplex virus, immune system, immune response, vaccine. 40 Years after the Registration of Acyclovir: Do We Need New Anti-Herpetic Drugs? Health Sci. Learn about how herpes affects the eyes and what treatments are available to, Medical News Today has strict sourcing guidelines and draws only from peer-reviewed studies, academic research institutions, and medical journals and associations. Therapeutics to prevent cold sores is not something that will emerge in the near future, due to the complexities involved in creating a drug specific enough to only affect certain transporters. Safety and immunogenicity of a glycoprotein D genital herpes vaccine in healthy girls 1017 years of age: Results from a randomized, controlled, double-blind trial. Intramuscular delivery of replication-defective herpes simplex virus gives antigen expression in muscle syncitia and improved protection against pathogenic HSV-2 strains. This function is dependent upon the degradation of ND10 constituent proteins (PML and SP100) using its ubiquitin ligase activity [15,17,18]. The ICP0 protein mutant HSV-1 has been reported to have a low growth rate. Financial support for ScienceDaily comes from advertisements and referral programs, where indicated. Vaselenak R.L., Shlapobersky M., Pyles R.B., Wei Q., Sullivan S.M., Bourne N. A vaxfectin ()-adjuvanted HSV-2 plasmid DNA vaccine is effective for prophylactic and therapeutic use in the guinea pig model of genital herpes. 2022 Mar 23;96(6):e0172421. It was reported that the phosphorylation of this ICP0 motif by host kinase Chk2 increases the potency of ICP0 to act as a SUMO targeted ubiquitin ligase [STUbl]. Herpes simplex virus 2 (HSV-2) infected cells proteins are among the most dominant antigens of a live-attenuated HSV-2 vaccine. The K-27 and K-63 call upon the TBK1, which is a kinase that will phosphorylate STING. Unterholzner L., Keating S.E., Baran M., Horan K.A., Jensen S.B., Sharma S., Siros C.M., Jin I., Latz E., Xiao T.S., et al. WebYou're most at risk of complications from the virus if you have a weak immune system from conditions and treatments such as: HIV/AIDS. It also reduces inflammation, pain, and other cold sore symptoms. Ectopic expression of VP22 was said to decrease cGAS/STING-mediated IFN- promoter activation and expression of IFN- [86]. It was reported that HSV-1 infection led to the activation of apoptosis with accompanying golgi fragmentation and downregulation of occludin and claudin 5. Everything You Should Know About Yoni Pearls. Cancer Toll-like receptors 2 and 3 have been reported to play a role in sensing HSV-1 and the activation of interferon type 1 and inflammatory cytokines [13]. Glycoprotein G of herpes simplex virus 2 as a novel vaccine antigen for immunity to genital and neurological diseases. van Lint A.L., Murawski M.R., Goodbody R.E., Severa M., Fitzgerald K.A., Finberg R.W., Knipe D.M., Kurt-Jones E.A. Note: Content may be edited for style and length. A weakened immune system makes herpes outbreaks more likely. ICP0 is an E3 ubiquitin ligase comprising 775 amino acids with an N-terminal RING structure [17]. doi: 10.1093/infdis/jit458. It is broadly divided into two, namely, the structural component (anatomical barrier) and chemical component. Prophylactic vaccines for HSV are needed to effectively stimulate primary immune responses at the site of pathogen entry, involving the nave T cells of which the DCs are the important cell type for stimulating nave T and B cells [144], thereby protecting uninfected hosts. Should I Be Worried If I Have An Itchy Clitoris? Kim C.H., Oh S.D., Park H.J., Kim H., Seo Y.B., Yoo J.H., Jang S.H., Shin J., Kim W.C., Kwon S.M., et al. It has been suggested that HSV-induced Dok phosphorylation and Dok-2 degradation could be a strategy of immune evasion to inactivate T-cells, which might play a role in HSV pathogenesis [85]. Rockefeller University. Five miRNAs (miR-H3, miR-H4-3p, miR-H4-5p, miR-H24, and miR-H19) encoded by latency associated transcript RLI sequence are implicated due to the overexpression of miR-H3, miR-H4-5p and miR-H19 in PC12 cells [97]. J. Infect. Overall, we can safely say that herpes can disrupt the way our immune system functions. We know our bodies better than anybody else, so make sure to listen to your instincts and ask a professional what you dont already know. If you have a strong immune system can it fight herpes? - Quora Histone chaperone HIRA deposits histone H3.3 onto foreign viral DNA and contributes to anti-viral intrinsic immunity. On the other hand, immunotherapeutic vaccines are also important to reduce herpes shedding and alleviate herpetic disease in symptomatic patients with recurrent outbreaks [8]. When your immune system isnt functioning properly, VZV can reactivate. It has been reported that the vaccine significantly protected new-born mice from neonatal HSV, and showed that the neonatal protection was a consequence of the new-borns acquiring antibodies that mediate ADCC from the mother transplacentally and through breastfeeding [151]. An official website of the United States government. Herpes Gu H. What role does cytoplasmic ICP0 play in HSV-1 infection? In other words, herpesviruses prevent alarming our cells about the infection, allowing the virus to spread in our system and hide from our immune system. The new study investigates in detail how HSV-1 manages to do this and evade detection by the immune system, which normally spots cells behaving abnormally and kills them before they can do too much damage. Akhrameyeva N.V., Zhang P., Sugiyama N., Behar S.M., Yao F. Development of a glycoprotein D-expressing dominant-negative and replication-defective herpes simplex virus 2 (HSV-2) recombinant viral vaccine against HSV-2 infection in mice. Can diet and exercise reverse prediabetes? 2015;15:737747. The innate immune system is the first point of defence in eukaryotic organisms; it is usually fast and non-specific. Zhao Y., Yang J., Liu Y., Fan J., Yang H. HSV-2-encoded miRNA-H4 regulates cell cycle progression and Act-D-induced apoptosis in HeLa cells by targeting CDKL2 and CDKN2A. On the premise that prophylactic and immunotherapeutic vaccines have different goals and initiate different immune responses (carefully discussed by Truong et al. WebVirgin's team found that one type of herpes virus makes its own version of RCA to trick the immune system and evade destruction by complement, but that the RCA mimic proteins Viruses like HSV-1 can remain dormant in their hosts for a long time and then flare up again. Xu X., He Y., Fan S., Feng M., Jiang G., Wang L., Zhang L., Liao Y., Qihan L. Reducing viral inhibition of host cellular apoptosis strengthens the immunogenicity and protective efficacy of an attenuated HSV-1 strain. February 17, 2022. This virus can lead to a sore throat, blisters in the mouth or genital organs, along with various other symptoms. Overview of the immune response. Mayo Clinic Minute: How to maintain a healthy immune system It is critical to consider the mechanisms by which HSV evades the immune system during the process of designing and administration of different vaccine compounds and formats [45]. On the contrary, higher wild-type virus yields were observed in SP100-/-infected cells than in the parental Hep-2 cells at low multiplication of infection [60]. Aubert M., Krantz E.M., Jerome K.R. They constitute the first line of defence against pathogens. Updated: September 8, 2022 By Steve S Boosting Your Immune System Describe the New Genital Herpes Therapeutic Vaccine and How it Works Another way to potentially speed up healing for herpes outbreaks and reduce the frequency of future outbreaks is to strengthen your bodys natural immunity. Common symptoms of the herpes virus include a tingling sensation around the mouth or genitals followed by sores. This will repress the transcription of genes involved in inflammatory reactions. ICP0 is a promiscuous transactivator of HSV-1 immediateearly, early and late genes [16]. However, despite the development and trial of many vaccines, this has not yet been possible. Your Immune System: Things That Can Weaken It - WebMD TAP is a member of a family of transporters that are found across human cells, a number of which pump molecules like nutrients and drugs across membranes to various cellular compartments. 2014;209:325333. STING can also recruit TRAF6 to activate the transcription factor NF-B for expression of genes involved in inflammatory response [40]. What Causes Shingles to Activate and What to Do About It Viruses are not like cells they have DNA, but no machinery. Zhang C., Shang G., Gui X., Zhang X., Bai X.C., Chen Z.J. VP24 protein was reported to dampen interferon stimulatory DNA (ISD)-triggered IFN- production and inhibit IFN- promoter activation induced by cyclic cGAS and STING [91]. Although it is already in our bodies, herpesviruses do not necessarily harm most of the time. It has been suggested through further studies that VP22 interacts with cGAS and inhibit its enzymatic activity. Lysozyme as an alternative to growth promoting antibiotics in swine production. The PML-NBs is organized by proteinprotein interaction between SUMOylated proteins and SUMO-interacting motifs (SIMs) [61]. Davido D.J., Tu E.M., Wang H., Korom M., Casals A.G., Reddy P.J., Mostafa H.H., Combs B., Haenchen S.D., Morrison L.A. Attenuated herpes simplex virus 1 (HSV-1) expressing a mutant form of ICP6 stimulates a strong immune response that protects mice against HSV-1 induced corneal disease. Host-encoded miR-649 was reported to promote HSV-1 replication through regulation of the mucosa-associated lymphoid tissue lymphoma translocation gene 1 (MALT1)-mediated antiviral signalling pathway [99]. 2023 Apr 20;23(1):230. doi: 10.1186/s12903-023-02924-0. Xu X., Zhang Y., Qihan L. Characteristics of herpes simplex virus infection and pathogenesis suggest a strategy for vaccine development. The herpes simplex virus 1 immediate early protein ICP22 is a functional mimic of a cellular J protein. Researchers have now found a mechanism that appears to explain, Herpes antibodies occur once a person contracts the herpes virus. official website and that any information you provide is encrypted The cellular equivalent of these are proteins the workhorses that carry out all the cell functions. Our DNA code contains the instructions for making all the cells of our whole body, and the work that they do. Taking a working copy of a gene for making a protein is called transcription. Viruses. Another challenge is the uncertainty of the humoral and cell-mediated responses induced by HSV vaccine candidates to confer lasting protection. HSV-1 also exploits the anterograde transport mechanism [84] in cells to move viral particles from neuron cell bodies to axon tips during reactivation of infection, and this is implicated in the spread of viral particles in epithelial tissues and general dissemination of the virus to other hosts. doi: 10.1080/20477724.2019.1678938. Rubio R.M., Mohr I. Inhibition of ULK1 and Beclin1 by an -herpesvirus Akt-like Ser/Thr kinase limits autophagy to stimulate virus replication. Numerous immune cells, particularly the natural killer cells and interferon gamma and pathways that are used by the body to fight HSV infections have been identified. Bernstein D.I., Wald A., Warren T., Fife K., Tyring S., Lee P., Wagoner N.V., Margaret A., Flechtner J.B., Tasker S., et al. Enk J., Levi A., Weisblum Y., Yamin R., Charpak-Amikam Y., Wolf D.G., Mandelboim O. HSV1 microRNA modulation of GPI anchoring and downstream immune evasion. How herpes virus tricks the immune system -- ScienceDaily One of the senior investigators, Professor Lars Dlken from Cambridges department of medicine and Wrzburgs institute of virology, describes the effect HSV-1 has on the hosts transcription process: Its like someone transcribing a short story, but instead of stopping at The End, they carry on and transcribe all the copyright and publication details and ISBN numbers at the beginning and end of the book. Rockefeller University. WebPeople with a weak immune system have a higher risk of experiencing frequent infections and severe symptoms. Kao C.M., Goymer J., Loh L.N., Mahant A., Aschner B.C., Herold B.C. Scientists are still studying why this happens. "Once this virus enters the body, it never leaves. Scientists reveal how herpes virus hijacks and hides in our cells Factors The skin provides an outer impermeable cover against invasion by pathogens [9]. But once our bodies receive an external alarm such as stress and weakening, that is when the virus awakens, and the immune system starts to fight it off. Su C., Zhan G., Zheng C. Evasion of host antiviral innate immunity by HSV-1, an update recruitment of the downstream adaptor TBK1. Following the successful development and use of vaccine against varicella zoster virus, a closely related virus in the same viral family, there has been a recent upsurge of interest in developing vaccine against HSV. The virus selectively targets lamin A/C, B1, and B2 for degradation, which then facilitates the egress of newly formed infectious particles. Effects of HIV on the Body: Virus and Medications - WebMD Explaining whether or not herpes can weaken or boost the immune system is not as simple as you think it may be. The chemicals components include, the lysozyme, defensins, interleukin, interferon, and complement proteins.