scholarly journals Arenavirus-Mediated Liver Pathology: Acute Lymphocytic Choriomeningitis Virus Infection of Rhesus Macaques Is Characterized by High-Level Interleukin-6 Expression and Hepatocyte Proliferation

2003 ◽  
Vol 77 (3) ◽  
pp. 1727-1737 ◽  
Author(s):  
Igor S. Lukashevich ◽  
Ilia Tikhonov ◽  
Juan D. Rodas ◽  
Juan C. Zapata ◽  
Yida Yang ◽  
...  
Keyword(s):  
Virus Infection ◽  
Liver Regeneration ◽  
Interleukin 6 ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Rhesus Macaques ◽  
Acute Infection ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Hepatocyte Proliferation

ABSTRACT Lymphocytic choriomeningitis virus (LCMV) and Lassa virus can cause hemorrhagic fever and liver disease in primates. The WE strain of LCMV (LCMV-WE) causes a fatal Lassa fever-like disease in rhesus macaques and provides a model for arenavirus pathogenesis in humans. LCMV-WE delivered intravenously or intragastrically to rhesus macaques targets hepatocytes and induces high levels of liver enzymes, interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and soluble tumor necrosis factor receptors (sTNFRI and -II) in plasma during acute infection. Proinflammatory cytokines TNF-α and IL-1β were not detected in plasma of infected animals, but increased plasma gamma interferon was noted in fatally infected animals. Immunohistochemistry of acute liver biopsies revealed that 25 to 40% of nuclei were positive for proliferation antigen Ki-67. The increases in IL-6, sIL-6R, sTNFR, and proliferation antigen that we observe are similar to the profile of incipient liver regeneration after surgical or toxic injury (N. Fausto, Am. J. Physiol. 277:G917-G921, 1999). Although IL-6 was not directly induced by virus infection in vitro, peripheral blood mononuclear cells from acutely infected monkeys produced higher levels of IL-6 upon lipopolysaccharide stimulation than did healthy controls. Our data confirm that acute infection is associated with weak inflammatory responses in tissues and initiates a program of liver regeneration in primates.

scholarly journals Integrated cytokine and metabolite analysis reveals immunometabolic reprogramming in COVID-19 patients with therapeutic implications

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nan Xiao ◽  
Meng Nie ◽  
Huanhuan Pang ◽  
Bohong Wang ◽  
Jieli Hu ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Ex Vivo ◽  
Rhesus Macaques ◽  
Fatal Outcome ◽  
Organ Injury ◽  
Cytokine Release ◽  
Serum Samples ◽  
Peripheral Blood Mononuclear

AbstractCytokine release syndrome (CRS) is a major cause of the multi-organ injury and fatal outcome induced by SARS-CoV-2 infection in severe COVID-19 patients. Metabolism can modulate the immune responses against infectious diseases, yet our understanding remains limited on how host metabolism correlates with inflammatory responses and affects cytokine release in COVID-19 patients. Here we perform both metabolomics and cytokine/chemokine profiling on serum samples from healthy controls, mild and severe COVID-19 patients, and delineate their global metabolic and immune response landscape. Correlation analyses show tight associations between metabolites and proinflammatory cytokines/chemokines, such as IL-6, M-CSF, IL-1α, IL-1β, and imply a potential regulatory crosstalk between arginine, tryptophan, purine metabolism and hyperinflammation. Importantly, we also demonstrate that targeting metabolism markedly modulates the proinflammatory cytokines release by peripheral blood mononuclear cells isolated from SARS-CoV-2-infected rhesus macaques ex vivo, hinting that exploiting metabolic alterations may be a potential strategy for treating fatal CRS in COVID-19.

scholarly journals Lymphocytic Choriomeningitis Virus Infection in FVB Mouse Produces Hemorrhagic Disease

2012 ◽  
Vol 8 (12) ◽  
pp. e1003073 ◽  
Author(s):  
Frederick J. Schnell ◽  
Sarah Sundholm ◽  
Stacy Crumley ◽  
Patrick L. Iversen ◽  
Dan V. Mourich
Keyword(s):  
Virus Infection ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Hemorrhagic Disease ◽  
Lymphocytic Choriomeningitis Virus Infection

Behavioral effects of persistent lymphocytic choriomeningitis virus infection in mice

1994 ◽  
Vol 62 (2) ◽  
pp. 100-109 ◽  
Author(s):  
Lisa H. Gold ◽  
Michelle D. Brot ◽  
Ilham Polis ◽  
Richard Schroeder ◽  
Antoinette Tishon ◽  
...  
Keyword(s):  
Virus Infection ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Behavioral Effects ◽  
Lymphocytic Choriomeningitis Virus Infection

scholarly journals IMMUNOPATHOLOGY OF LYMPHOCYTIC CHORIOMENINGITIS VIRUS INFECTION OF NEWBORN MICE

1968 ◽  
Vol 127 (4) ◽  
pp. 757-766 ◽  
Author(s):  
Martin S. Hirsch ◽  
Frederick A. Murphy ◽  
Martin D. Hicklin
Keyword(s):  
Virus Infection ◽  
Antibody Formation ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Reticular Cell ◽  
Wasting Disease ◽  
Cell Hyperplasia ◽  
Newborn Mice ◽  
Lymphocytic Choriomeningitis Virus Infection ◽  
Cellular Tolerance

Antithymocyte serum, when administered neonatally to mice, delayed the maturation of the lymphoid system, permitting development of cellular tolerance to LCM virus at an older age than is ordinarily possible. Humoral antibody formation was not prevented and the animals exhibited the paradox of high titers of both circulating virus and antibody. This, in turn, was followed by a chronic immunopathologic glomerulonephritis in most animals. Some animals developed wasting disease between 1 and 2 months of age, characterized by reticular cell hyperplasia and widespread infiltration into tissues and organs.

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