scholarly journals A Case of Disseminated Cutaneous Herpes Simplex Virus-1 as the First Manifestation of Human Immunodeficiency Virus Infection

2021 ◽  
Vol 9 ◽  
pp. 232470962110452
Author(s):  
Parker Brown ◽  
Sandra Elmasry ◽  
Abdulbaril Olagunju ◽  
Santiago Garcia ◽  
Mansi Sarihan

Reported clinical manifestations of active herpes simplex virus type 1 (HSV-1) infection include typically painful vesicular cutaneous rash in a dermatomal distribution, temporal lobe encephalitis, and rarely, fulminant septic shock with multiorgan failure. In immunocompromised patients, the cutaneous rash can become disseminated. We report a case of a 33-year-old male patient with undiagnosed human immunodeficiency virus (HIV) infection who presented to our emergency department (ED) with a disseminated cutaneous rash. The rash was extensive, involved 90% of his total body surface area. It began 5 days prior as small ulcerations localized to the left arm, sought care at an outside ED, diagnosed as severe dermatitis with bacterial superinfection and discharged with a cephalexin prescription. Laboratory results were positive for HIV test with a CD4 count of 254, white blood cell count (WBC) of 7.4 k/microL with 54% neutrophils, 9% lymphocytes, 0% eosinophils, 0% basophils, and serum creatinine and sodium of 3.05 mg/dL and 119 mEq/L, respectively. The burn team and dermatology ruled out Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis due to the absence of mucosal involvement, negative nikolsky sign, and absence of skin sloughing. Polymerase chain reaction of samples obtained from the skin lesions was positive for HSV-1. The rash resolved with intravenous acyclovir and was started on highly active antiretroviral therapy (HAART) on outpatient follow-up. To the best of our knowledge, comparable cases of significantly disseminated cutaneous HSV-1 infection as the initial presentation of HIV infection have been rarely reported.

2017 ◽  
Vol 92 (2) ◽  
Author(s):  
Sachith Polpitiya Arachchige ◽  
Wyatt Henke ◽  
Ankita Pramanik ◽  
Maria Kalamvoki ◽  
Edward B. Stephens

ABSTRACTVirus-encoded proteins that impair or shut down specific host cell functions during replication can be used as probes to identify potential proteins/pathways used in the replication of viruses from other families. We screened nine proteins from herpes simplex virus 1 (HSV-1) for the ability to enhance or restrict human immunodeficiency virus type 1 (HIV-1) replication. We show that several HSV-1 proteins (glycoprotein M [gM], US3, and UL24) potently restricted the replication of HIV-1. Unlike UL24 and US3, which reduced viral protein synthesis, we observed that gM restriction of HIV-1 occurred through interference with the processing and transport of gp160, resulting in a significantly reduced level of mature gp120/gp41 released from cells. Finally, we show that an HSV-1 gM mutant lacking the majority of the C-terminal domain (HA-gM[Δ345-473]) restricted neither gp160 processing nor the release of infectious virus. These studies identify proteins from heterologous viruses that can restrict viruses through novel pathways.IMPORTANCEHIV-1 infection of humans results in AIDS, characterized by the loss of CD4+T cells and increased susceptibility to opportunistic infections. Both HIV-1 and HSV-1 can infect astrocytes and microglia of the central nervous system (CNS). Thus, the identification of HSV-1 proteins that directly restrict HIV-1 or interfere with pathways required for HIV-1 replication could lead to novel antiretroviral strategies. The results of this study show that select viral proteins from HSV-1 can potently restrict HIV-1. Further, our results indicate that the gM protein of HSV-1 restricts HIV-1 through a novel pathway by interfering with the processing of gp160 and its incorporation into virus maturing from the cell.


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