Viral Genetic Diversity and Its Potential Contributions to the Development and Progression of Neonatal Herpes Simplex Virus (HSV) Disease

Akhtar, Lisa N.; Szpara, Moriah L.

doi:10.1007/s40588-019-00131-6

Cited by 4 publications

(2 citation statements)

References 54 publications

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“…Herpes simplex virus (HSV, including HSV‐1 and HSV‐2) is one of the human herpes viruses (HHV) whose infection is common 10 . Manifestation of HSV also varied among many studies due to stress, viral genetic diversity, and immune responses 11–13 . The infection with HSV‐1 and HSV‐2 can be asymptomatic, mild, or life‐threatening, depending on the interaction between HSV and the host, particularly with the immune system.…”

Section: Introductionmentioning

confidence: 99%

“…10 Manifestation of HSV also varied among many studies due to stress, viral genetic diversity, and immune responses. [11][12][13] The infection with HSV-1 and HSV-2 can be asymptomatic, mild, or life-threatening, depending on the interaction between HSV and the host, particularly with the immune system. The HSV infection could create significant complications in the immunocompromised host.…”

Section: Introductionmentioning

confidence: 99%

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Mendelian randomization analysis suggests no associations of herpes simplex virus infections with systemic lupus erythematosus

Chang

Liu

Chen

et al. 2023

Journal of Medical Virology

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Systemic lupus erythematosus (SLE) characterized by immune dysfunction is possibly more vulnerable to herpes simplex virus (HSV) infection. The infection has been intensively considered a common onset and exacerbation of SLE. This study is aimed at elucidating the causal association between SLE and HSV. A bidirectional two‐sample Mendelian Randomization (TSMR) analysis was systematically conducted to explore the causal effect of SLE and HSV on each other. The causality was estimated by inverse variance weighted (IVW), MR‐Egger and weighted median methods based on the summary‐level genome‐wide association studies (GWAS) data from a publicly available database. Genetically proxied HSV infection exhibited no causal association with SLE in the forward MR analysis using IVW method (odds ratio [OR] = 0.987; 95% confidence interval [CI]: 0.891–1.093; p = 0.798), nor did HSV‐1 IgG (OR = 1.241; 95% CI: 0.874–1.762; p = 0.227) and HSV‐2 IgG (OR = 0.934; 95% CI: 0.821–1.062; p = 0.297). Similar null results with HSV infection (OR = 1.021; 95% CI: 0.986–1.057; p = 0.245), HSV‐1 IgG (OR = 1.003; 95% CI: 0.982–1.024; p = 0.788) and HSV‐2 IgG (OR = 1.034; 95% CI: 0.991–1.080; p = 0.121) were observed in the reverse MR where SLE served as the exposure. Our study demonstrated no causal association between the genetically predicted HSV and SLE.

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Section: Introductionmentioning

confidence: 99%