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Introduction
Herpes simplex virus 2 (HSV-2) is a virus that causes genital herpes. It belongs in the same genus and family with herpes simplex virus 1. The virus has several mechanisms that enhance its virulence. Its interaction with the immune system is complex, thus rendering the development of a vaccine difficult. Treatment involves the administration of antiviral drugs, even though drug resistance is encountered sometimes. Infection can be prevented by using condoms during sexual intercourse and abstaining from vaginal, anal, and oral sex.
Description of Organism
Herpes simplex virus 2 (HSV-2), taxonomically referred to as the alphaherpesvirus 2 is a virus that causes genital herpes. It belongs to the Herpesviridiae family, the Herviviricetes class, and the simplexvirus genus. It belongs to the same family as simplex virus 1 that also causes herpes. HSV-2 is a large, spherical, double stranded DNA virus that comprises a four-layered structure: a core, a capsid, an envelope, and a tegument (Serdaroglu, & Kutlubay, 2017). It is wrapped in a protein cage called a capsid, which is surrounded by a lipid bilayer, commonly referred to as the envelope (Tognarelli et al., 2019). The capsid and the envelope are joined together by means of a tegument. The virus contains approximately 74 genes that encode proteins that form the capsid, the envelope, and the tegument. In clinical tests, quantitative real-time polymerase chain reaction (qPCR) is to detect the virus (Tognarelli et al., 2019). Gram staining techniques are usually used for detecting bacteria and fungi, and they are usually ineffective in the diagnosis of viral infections because viruses lack the cell wall.
Virulence factors
The HSV-2 has undergone evolution for thousands of years, and their prevalence in the population is relatively high. The virus has the ability to persist and recur in healthy individuals because of the virulence factors that they have evolved over the years. These viruses cause lifelong infections because of their ability to establish latency in neurons and subsequent reactivation that is associated with episodes of viral shedding. Their virulence factors include interfering with toll-like receptor sensing functions, hampering the ability of non-Toll-like receptors (TLRs) to identify viral nucleic acids, interfering with the hosts interferon response, and down-modulating the activities of innate immune cells (Tognarelli et al., 2019). The infected cell protein (ICP) 34.5 prevents the maturation of dendritic cells while surface glycoproteins on the viral envelope mimic host cells to avoid activation and elimination (Zhu & Viejo-Borbolla, 2021).
Molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) are sensed by structures known as Toll-like receptors (TLRs), which initiate the expression of antiviral activity. HSV-2 interferes with the functioning of these receptors, thus rendering the host unable to recognize viral infection (Tognarelli et al., 2019). Viral nucleic acids play an important role in immunity because they activate signaling pathways that initiate antiviral responses against infections. HSV-2 is highly virulent because it hampers the ability of non-TLR receptors to recognize the nucleic acids of viruses after infection. HSV-2 also interferes with the host interferon response by encoding several molecular factors that affect the production, secretion, and the activity of interferons (IFNs) (Tognarelli et al., 2019). Interferons play a key role in fighting infections by triggering antiviral responses that prevent the replication of viruses. HSV-2 also inhibits the proper functioning of innate immune cells and the complement system (Tognarelli et al., 2019). The virus stops the reactions of the complement system by preventing protein activations that are important in the formation of a membrane attack complex (MAC) on the pathogens surface or infected cells.
Immunity
The Innate and the adaptive immune systems are responsible for protecting individuals against HSV-2 infections. The innate immune system is a fast and non-specific defense mechanism that includes the skin and the mucus membrane (Ike et al., 2020). Secretions such as fatty acids and sweat are toxic to pathogens. The adaptive immune system is more effective because of its specificity and memory properties. The system is primarily comprised of T-lymphocytes that oversee the cellular immune response and B-lymphocytes that secrete antibodies and mediate the humoral immune response (Ike et al., 2020).
Infectious Disease Information
HSV-2 causes genital herpes, a disease that is characterized by blisters or lesions that appear on the surface of the mouth, rectum, or genitals. Tender sores appear after the lesions break, prior to which the individual experiences a burning or itching sensation (Serdaroglu, & Kutlubay, 2017). In certain cases, the disease is asymptomatic. However, in cases where symptoms appear, genital or anal blisters are observed. Complications that could develop if the disease is untreated include bladder problems, meningitis, yeast infections, rectal inflammation (proctitis), and sexually transmitted diseases such as AIDS.
Epidemiology
The virus infects more than 500 million people across the globe, with approximately 50 million coming from the United States. The transmission of HSV-2 occurs through sexual contact with the genitals, skin, or anal surfaces of an infected individual. The virus can be transmitted, even though the skin does not have lesions as it is transferred between hosts without the presence of symptoms (Serdaroglu, & Kutlubay, 2017). In some cases, HSV-2 is shed in the genital tract, and transmitted during sexual intercourse. Moreover, transmission occurs through contact with a herpes sore, genital fluids from an infected person, and saliva from an infected person (Serdaroglu, & Kutlubay, 2017). The virus cannot be transmitted by touching the surfaces of objects such as toilet seats and beddings.
Prevention
Scientists have conducted several clinical tests for vaccines against genital herpes. However, none of them has been successful so far. In that regard, the unavailability of a vaccine means that individuals have to use preventive means to avoid infection. The two main strategies for the prevention of genital herpes are sexual abstinence and the use of protection during intercourse (Serdaroglu, & Kutlubay, 2017). The avoidance of vaginal, anal, and oral sex is the most effective preventative measure against genital herpes. Another strategy is the practice of monogamy; sexually active people should ensure that they remain monogamous and use condoms during intercourse (Serdaroglu, & Kutlubay, 2017). In certain cases, condoms could be ineffective because the skin can shed the virus in areas that do not have sores. In that regard, condoms are effective only in cases that involve transmission through the male sexual organ.
Treatment
Genital herpes does not have a specific eradication modality. However, there are three classes of drugs that are used for treatment purposes: acyclic guanosine analogues, pyrophosphate analogues, and nucleotide analogues. The treatment of the disease involves the administration of antiviral drugs that interfere with the replication of the virus and shorten outbreaks (Serdaroglu, & Kutlubay, 2017). Moreover, they mitigate the severity of lesions and reduce the risk of transmission to healthy individuals. Studies conducted have shown that the use of drugs such as acyclovir and valaciclovir on a daily basis lowers the rate of viral activation (Serdaroglu, & Kutlubay, 2017). Treatment failure usually results from the development of drug resistance due to the prolonged use of a specific drug. The administration of antiviral medicines is the only remedy because a vaccine to prevent infection has not yet been developed. The vaccines that have been tried have not shown any substantive results, hence they cannot be approved for use.
Clinical Relevance
HSV-2 is effectively treated using antiviral drugs such as acyclovir. However, resistance to the drug has been reported in certain cases. Immunocompromised individuals and patients who have undergone allogeneic bone marrow transplant have shown resistance to the drug, thus rendering treatment ineffective (Serdaroglu, & Kutlubay, 2017). This is due to mutations on either thymidine kinase (TK) or DNA polymerase. In the majority of the reported cases, resistance to ACV is caused by mutation in the TK genes (Serdaroglu, & Kutlubay, 2017). Research has shown that this challenge can be mitigated by using another type of medication that has a different mechanism of action. The effects of resistance include more severe infections among immunocompromised patients. It is important for scientists to develop more effective methods of detecting resistance to antiviral drugs for improved health outcomes.
Conclusion
HSV-2 is a virus that causes genital herpes and that establishes latency in neurons, therefore reactivating and causing new infections. Infected individuals experience sores or lesions on infected regions. Transmission occurs through contact with the genitals or the skin of an infected individual. Moreover, transmission occurs through contact with a herpes sore, genital fluids, and saliva from an infected person. The virus infects more than 500 million people worldwide. Treatment involves the administration of antiviral drugs that prevent viral replication. A vaccine has not yet been developed, though several have unsuccessfully undergone clinical trials.
References
Ike, A. C., Onu, C. J., Ononugbo, C. M., Reward, E. E., and Muo, S. O. (2020). Immune response to Herpes simplex virus infection and vaccine development. Vaccines, 8(2), 302. Web.
Serdaroglu, S., & Kutlubay, Z. (Eds.). (2017). Fundamentals of sexually transmitted infections. Books on Demand.
Tognarelli, E. I., Palomino, T. F., Corrales, N., Bueno, S. M., Kalergis, A. M., and Gonzalez, P. A. (2019). Herpes simplex virus evasion of early host antiviral responses. Frontiers in Cellular and Infection Microbiology, 9 (127), 1-24. Web.
Zhu, S., & Viejo-Borbolla, A. (2021). Pathogenesis and virulence of herpes simplex virus. Virulence, 12(1), 2670-2702. Web.
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