scholarly journals First description of single-pass albumin dialysis combined with cytokine adsorption in fulminant liver failure and hemophagocytic syndrome resulting from generalized herpes simplex virus 1 infection

2014 ◽  
Vol 20 (12) ◽  
pp. 1523-1524 ◽  
Author(s):  
Silvius Frimmel ◽  
Jan Schipper ◽  
Joerg Henschel ◽  
Tsui Tung Yu ◽  
Steffen R. Mitzner ◽  
...  
Author(s):  
Stefano Busani ◽  
Andrea Bedini ◽  
Emanuela Biagioni ◽  
Lucia Serio ◽  
Roberto Tonelli ◽  
...  

Abstract We reported two fatal cases of acute liver failure secondary to Herpes Simplex Virus 1 infection in COVID-19 patients, following tocilizumab and corticosteroid therapy.Screening for and prompt recognition of Herpes Simplex Virus 1 reactivation in these patients, undergoing immunomodulatory treatment, may have potentiallyrelevant clinical consequences.


1995 ◽  
Vol 14 (3) ◽  
pp. 242-243 ◽  
Author(s):  
David S. Greenes ◽  
David Rowitch ◽  
Grace M. Thorne ◽  
Antonio Perez-Atayde ◽  
Frank S. Lee ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Ashwinee Natu ◽  
Guiseppe Iuppa ◽  
Clifford D. Packer

Objective. To compare three cases of Herpes simplex virus (HSV) hepatitis to increase early diagnosis of the disease. Case  1. A 23-year-old man with Crohn’s disease and oral HSV. HSV hepatitis was diagnosed clinically and he improved with acyclovir. Case  2. An 18-year-old G1P0 woman with transaminitis. Despite early empiric acyclovir therapy, she died due to fulminant liver failure. Case  3. A 65-year-old woman who developed transaminitis after liver transplant. Diagnosis was confirmed by biopsy and she had resolution of acute liver failure with acyclovir. Conclusion. It is imperative that clinicians be aware of patients at high risk for developing HSV hepatitis to increase timely diagnosis and prevent morbidity and fatality.


Infection ◽  
2010 ◽  
Vol 38 (5) ◽  
pp. 423-426 ◽  
Author(s):  
A. Cusini ◽  
H. F. Günthard ◽  
G. Stussi ◽  
U. Schwarz ◽  
T. Fehr ◽  
...  

2019 ◽  
Vol 6 (11) ◽  
Author(s):  
Kevin Ikuta ◽  
Pavitra Roychoudhury ◽  
Hong Xie ◽  
Christopher L Mcclurkan ◽  
Magdalena Walkiewicz ◽  
...  

Abstract We describe a case of acute liver failure and myopericarditis due to herpes simplex virus–1 (HSV-1) in an immunocompetent adult. We estimate that, at the height of viremia, the patient contained a quantity of HSV-1 virions approaching that of human cells. The patient recovered with acyclovir that was dose-adjusted for neurotoxicity and developed a vigorous anti-HSV-1 T-cell response.


2016 ◽  
Vol 90 (23) ◽  
pp. 10789-10799 ◽  
Author(s):  
Zachary M. Parker ◽  
Tracy Jo Pasieka ◽  
George A. Parker ◽  
David A. Leib

ABSTRACTThe interferon (IFN) response to viral pathogens is critical for host survival. In humans and mouse models, defects in IFN responses can result in lethal herpes simplex virus 1 (HSV-1) infections, usually from encephalitis. Although rare, HSV-1 can also cause fulminant hepatic failure, which is often fatal. Although herpes simplex encephalitis has been extensively studied, HSV-1 generalized infections and subsequent acute liver failure are less well understood. We previously demonstrated that IFN-αβγR−/−mice are exquisitely susceptible to liver infection following corneal infection with HSV-1. In this study, we used bone marrow chimeras of IFN-αβγR−/−(AG129) and wild-type (WT; 129SvEv) mice to probe the underlying IFN-dependent mechanisms that control HSV-1 pathogenesis. After infection, WT mice with either IFN-αβγR−/−or WT marrow exhibited comparable survival, while IFN-αβγR−/−mice with WT marrow had a significant survival advantage over their counterparts with IFN-αβγR−/−marrow. Furthermore, using bioluminescent imaging to maximize data acquisition, we showed that the transfer of IFN-competent hematopoietic cells controlled HSV-1 replication and damage in the livers of IFN-αβγR−/−mice. Consistent with this, the inability of IFN-αβγR−/−immune cells to control liver infection in IFN-αβγR−/−mice manifested as profoundly elevated aspartate transaminase (AST) and alanine transaminase (ALT) levels, indicative of severe liver damage. In contrast, IFN-αβγR−/−mice receiving WT marrow exhibited only modest elevations of AST and ALT levels. These studies indicate that IFN responsiveness of the immune system is a major determinant of viral tropism and damage during visceral HSV infections.IMPORTANCEHerpes simplex virus 1 (HSV-1) infection is an incurable viral infection with the most significant morbidity and mortality occurring in neonates and patients with compromised immune systems. Severe pathologies from HSV include the blindness-inducing herpetic stromal keratitis, highly debilitating and lethal herpes simplex encephalitis, and generalized infections that can lead to herpes simplex virus-induced acute liver failure. While immune compromise is a known factor, the precise mechanisms that lead to generalized HSV infections are unknown. In this study, we used and developed a mouse model system in combination with real-time bioluminescence imaging to demonstrate the relative importance of the immune and nonimmune compartments for containing viral spread and promoting host survival after corneal infection. Our results shed light on the pathogenesis of HSV infections that lead to generalized infection and acute liver failure.


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