BACKGROUND Hemophagocytic lymphohistiocytosis (HLH) and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) can trigger profound immune activation and systemic inflammation, leading to severe, often fatal, conditions. Simultaneously, HIV-infected patients, prone to immune dysregulation, face an increased risk of severe complications from SARS-CoV-2. The optimal timeline for initiating antiretroviral therapy (ART) in patients with severe SARS-CoV-2 and HIV co-infection, especially concerning the risk of HLH, remains uncertain. CASE REPORT We detail the case of a 47-year-old male with previously undiagnosed HIV who, following ART initiation, developed HLH amid SARS-CoV-2 co-infection. The patient also had biopsy-proven Kaposi Sarcoma with immunoreactivity to Human Herpesvirus 8 (HHV-8), detectable peripheral blood Epstein Barr virus (EBV) DNA PCR and Cytomegalovirus (CMV) DNA PCR, and suspected Pneumocystis jirovecii pneumonia. We believe these conditions contributed to the development of HLH. This case represents a unique report of multiple herpesviruses reactivation, acquired HLH during COVID-19 in a patient with previously undiagnosed HIV. Despite receiving ART, steroids, and appropriate antimicrobial therapy, the patient's condition did not improve. CONCLUSIONS Further research is required to understand immune dysregulation, including HLH, in patients with HIV and SARS-CoV-2 co-infection. The effects of ART initiation on treatment-naïve patients with potential concurrent opportunistic infections and/or herpesvirus reactivation warrant deeper examination to formulate clinical guidelines.
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http://dx.doi.org/10.12659/AJCR.939847 | DOI Listing |
PLoS Pathog
January 2025
Junior Research Group Herpesviruses, Infection Biology Unit, German Primate Center-Leibniz Institute for Primate Research, Göttingen, Germany.
Interaction with host cell receptors initiates internalization of Kaposi's sarcoma-associated herpesvirus (KSHV) particles. Fusion of viral and host cell membranes, which is followed by release of the viral capsid into the cytoplasm, is executed by the core fusion machinery composed of glycoproteins H (gH), L (gL), and B (gB), that is common to all herpesviruses. KSHV infection has been shown to be sensitive to inhibitors of vacuolar acidification, suggestive of low pH as a fusion trigger.
View Article and Find Full Text PDFExp Clin Transplant
December 2024
>From the Department of Nephrology and Transplantation, University Hospitals Plymouth, Plymouth; and the Department of Nephrology, University Hospitals Birmingham, Birmingham, UK.
Objectives: Cytomegalovirus infection is the most common opportunistic infection affecting organ transplant recipients and is associated with detrimental allograft and patient outcomes. In recipients previously seronegative for cytomegalovirus, acquired infection is termed primary infection, whereas infection acquired in recipients with previously confirmed seropositivity is called reactivation. Cytomegalovirus seropositivity carries a great risk of reactivation, and management for these patients may vary, from dug prophylaxis to pre emptive viral monitoring.
View Article and Find Full Text PDFGammaherpesviruses are oncogenic pathogens that establish lifelong infections. There are no FDA-approved vaccines against Epstein-Barr virus or Kaposi sarcoma herpesvirus. Murine gammaherpesvirus-68 (MHV68) infection of mice provides a system for investigating of gammaherpesvirus pathogenesis and testing vaccine strategies.
View Article and Find Full Text PDFCell Host Microbe
January 2025
Department of Biological Chemistry, Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address:
Jiang et al. investigate the role of the microbiota in postherpetic neuralgia (PHN), a chronic pain condition resulting from varicella-zoster virus reactivation. They identify microbiome alterations in PHN patients, linking microbes and pain sensitivity.
View Article and Find Full Text PDFSci Signal
January 2025
Department of Biomedical Engineering, Tufts University, Medford, MA 02155, USA.
Infection with herpes simplex virus type 1 (HSV-1) in the brains of carriers increases the risk of Alzheimer's disease (AD). We previously found that latent HSV-1 in a three-dimensional in vitro model of -heterozygous human brain tissue was reactivated in response to neuroinflammation caused by exposure to other pathogens. Because traumatic brain injury also causes neuroinflammation, we surmised that brain injury might similarly reactivate latent HSV-1.
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