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Herpes Simplex Type Two: Etiology

Intrinsic Etiology

The likelihood of infection by the same level of exposure to the virus differs among individuals. Further, among HIV-infected individuals, there is a differential rate of progression. Both depend on a number of factors related to the virus, host, and the environment. An individual’s genetic variability influences one’s vulnerability or resistance to the virus. There are three categories of host genes that have been reported to influence the rate of HIV progression; they include genes encoding cell-surface receptors. Others include genes found in the human beings’ leukocyte antigens responsible for regulating one’s immune response to an infection. The last category includes another cytokine, which are also referred to as the immune response genes. However, when it comes to herpes simplex -2 (HSV-2) no direct association between HSV-2 and virologic severity has been recorded; thus, the specific role of human variation in HSV-2 remains unclear (Kleinstein et al., 2019). However, it is evident that the presentation of herpes simplex type two among individuals depends on one’s immune status at the time of exposure.

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Extrinsic Etiology

Herpes complex as other related infections can be considered as a socio-economic challenge since its spread is linked to social and economic factors. Some of the aspects closely related to the spread of the virus include culture, religion, tradition, and poverty. An interplay of the elements plays a significant role in the development of the epidemic. For instance, where communities practice polygamy and wife inheritance, there is a likelihood of a relatively higher rate of herpes infections. Further, poverty is likely to lead to increased exposure and infection rates where individuals have to engage in sex for money so as to feed and cater to their other household needs. This probably explains why the rates of herpes simplex infections are higher in populations with lower socioeconomic status. These environmental influences can exacerbate people’s vulnerability to the virus or worsen the outcomes of the infection.

Other factors that have a direct influence of herpes simplex type two infection include an individual’s sex, race, age, and the level of education. Individuals with higher levels of education are more likely to understand the disease, particularly how it is spread, and thus take the necessary precautions to stay safe. Further, they are more likely to understand the severity of the infection and avoid risky sexual behavior that may lead to disease. Regarding age, the overall seroprevalence of the illness is higher among older patients compared to younger ones, including teenagers (Rawre et al., 2018). In terms of age, women are almost six times more likely to get herpes simplex type two infection compared to men for the same exposure levels (Rawre et al., 2018). Additionally, when considering race, black women are more likely to contract herpes simplex type two compared to other races, including whites and Asians. This might explain why the prevalence of herpes simplex two is unevenly distributed in different geographical regions.

Idiopathic Etiology

The etiology of herpes simplex type two is clear, with multiple studies indicating the various ways through which one might get infected. There are no documented unknown mechanisms or factors that may contribute to the disease. Further, it is unclear whether herpes simplex type two coinfection with HIV accelerates the severity of the latter. Additionally, it remains to be confirmed whether herpes simplex type two can be spread through water, such as in the case of type one.

References

Kleinstein S. E., Shea P. R., & Allen A. S. (2019). Genome-wide association study (GWAS) of human host factors influencing viral severity of herpes simplex virus type 2 (HSV-2). Genes and Immunity, 20(2), 112-120. Web.

Rawre, J., Rai, M., Namdeo, D., Das, R., Khanna, N., & Dar, L. (2018). Herpes simplex virus type 2 and cytomegalovirus perigenital ulcer in an HIV infected woman. Indian Journal of Medical Microbiology, 36(3), 441-443. Web.

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