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2. Human Acute and Chronic Viruses: Host-Pathogen Interactions and Therapeutics

Author

Hoffman, Matilde, Chigbu, DeGaulle I., Crumley, Brenndan L., Sharma, Ravi, Pustylnikov, Sergey, Crilley, Thomas, Ginwala, Rashida, Loonawat, Ronak, Joseph, Julie, Sales, Dominic, Wilson, Sydney, and Jain, Pooja

Subjects
Treatment, Viral infections, Viruses, T cells, chemical and pharmacologic phenomena, Dendritic cells, Article, Immunoprophylaxis
Abstract

Viruses are obligate intracellular pathogens that cause infection in susceptible host cells. Virus infections could be lytic, chronic, latent or immortalizing. Viruses causing latent infection are associated with high morbidity and mortality worldwide. The human body is protected from viral infection by physical and chemical barriers. However, when these barriers are breached, the body generates an antiviral immune response mediated by Natural killer (NK) cells, monocytes, Dendritic Cells (DCs), type I interferon (IFN), neutralizing antibodies, and T cells. DCs play an important role in generating a cell-mediated adaptive immune response to viruses, with conventional DCs playing a crucial role in the interactions between DCs and viruses. Crosstalk between NK cells and DCs facilitates DC maturation in antiviral innate immunity whereas crosstalk between DCs and T cells in antiviral adaptive immunity amplifies the function of mature DC. Viruses employ various strategies to evade the host immune system. They can block Pattern Recognition Receptors (PRRs) - mediated production of type I IFNs, inhibit maturation and functionality of DCs, and interfere with cell-mediated immunity. Here we will focus on important human disease-causing viruses including latest COVID19 that caused worldwide pandemic. Because of the high mortality rate associated with viral diseases, there is an urgent need to re-evaluate current antiviral agents with more research focusing on developing alternative anti-viral therapies with an enhanced therapeutic index and safety profiles. Future directions in approaching the development of vaccines should focus on specific vaccines that can induce CD8+T cell responses and produce IFN-gamma to promote a Th1-biased CD4+T-cell response.

Published
2020

4. Hepatitis C Virus Infection: Host⁻Virus Interaction and Mechanisms of Viral Persistence.

Author

Chigbu DI, Loonawat R, Sehgal M, Patel D, and Jain P

Subjects
Adaptive Immunity immunology, Antiviral Agents metabolism, Cytokines metabolism, Hepacivirus genetics, Hepacivirus pathogenicity, Hepatitis C virology, Hepatocytes metabolism, Humans, Immunity, Innate immunology, Interferons metabolism, Killer Cells, Natural immunology, Liver Cirrhosis immunology, Toll-Like Receptors metabolism, Hepacivirus metabolism, Hepatitis C immunology, Hepatitis C metabolism, Host Microbial Interactions physiology
Abstract

Hepatitis C (HCV) is a major cause of liver disease, in which a third of individuals with chronic HCV infections may develop liver cirrhosis. In a chronic HCV infection, host immune factors along with the actions of HCV proteins that promote viral persistence and dysregulation of the immune system have an impact on immunopathogenesis of HCV-induced hepatitis. The genome of HCV encodes a single polyprotein, which is translated and processed into structural and nonstructural proteins. These HCV proteins are the target of the innate and adaptive immune system of the host. Retinoic acid-inducible gene-I (RIG-I)-like receptors and Toll-like receptors are the main pattern recognition receptors that recognize HCV pathogen-associated molecular patterns. This interaction results in a downstream cascade that generates antiviral cytokines including interferons. The cytolysis of HCV-infected hepatocytes is mediated by perforin and granzyme B secreted by cytotoxic T lymphocyte (CTL) and natural killer (NK) cells, whereas noncytolytic HCV clearance is mediated by interferon gamma (IFN-γ) secreted by CTL and NK cells. A host-HCV interaction determines whether the acute phase of an HCV infection will undergo complete resolution or progress to the development of viral persistence with a consequential progression to chronic HCV infection. Furthermore, these host-HCV interactions could pose a challenge to developing an HCV vaccine. This review will focus on the role of the innate and adaptive immunity in HCV infection, the failure of the immune response to clear an HCV infection, and the factors that promote viral persistence.

Published
2019
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