scholarly journals HERC5 and the ISGylation Pathway: Critical Modulators of the Antiviral Immune Response

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1102
Author(s):  
Nicholas A. Mathieu ◽  
Ermela Paparisto ◽  
Stephen D. Barr ◽  
Donald E. Spratt
Keyword(s):  
Mammalian Cells ◽  
Drug Targets ◽  
Influenza A ◽  
Viral Infections ◽  
Viral Proteins ◽  
Viral Pathogens ◽  
Antiviral Immune Response ◽  
Immunodeficiency Virus ◽  
Interferon Stimulated Gene 15

Mammalian cells have developed an elaborate network of immunoproteins that serve to identify and combat viral pathogens. Interferon-stimulated gene 15 (ISG15) is a 15.2 kDa tandem ubiquitin-like protein (UBL) that is used by specific E1–E2–E3 ubiquitin cascade enzymes to interfere with the activity of viral proteins. Recent biochemical studies have demonstrated how the E3 ligase HECT and RCC1-containing protein 5 (HERC5) regulates ISG15 signaling in response to hepatitis C (HCV), influenza-A (IAV), human immunodeficiency virus (HIV), SARS-CoV-2 and other viral infections. Taken together, the potent antiviral activity displayed by HERC5 and ISG15 make them promising drug targets for the development of novel antiviral therapeutics that can augment the host antiviral response. In this review, we examine the emerging role of ISG15 in antiviral immunity with a particular focus on how HERC5 orchestrates the specific and timely ISGylation of viral proteins in response to infection.

scholarly journals Effects of APOBEC3G's Cytidine Deaminase Activity on Retroviral Evolution

2021 ◽  
Vol 15 ◽  
pp. 55-61
Author(s):  
Mary-Benedicta Obikili
Keyword(s):  
Viral Infection ◽  
Mammalian Cells ◽  
Viral Infections ◽  
Cytidine Deaminase ◽  
Viral Evolution ◽  
Cytidine Deaminase Activity ◽  
Immunodeficiency Virus ◽  
Potential Impact ◽  
Retroviral Infections

Apolipoprotein B editing complex (APOBEC3/A3) genes are found in mammalian cells. In primates, there are 7 APOBEC3 genes, namely, 3A, 3B, 3C, 3DE, 3F, 3G, and 3H. Previous research has shown that A3 proteins help to inhibit viral infection via their cytidine deaminase activity. However, it has also been found that A3 proteins could also lead to viral evolution, where viruses such as HIV (Human Immunodeficiency Virus) instead gain beneficial mutations that enable them to overcome the antiviral activity of A3 proteins, gain resistance to certain drugs used for treating viral infections and escape recognition by the immune system. This paper is a review article summarizing the role of A3G on viral infection and evolution, and the potential impact viral evolution could have in treatment of retroviral infections such as HIV.

scholarly journals Role of Viral Protein-Protein Interactions and Possible Targets for New Therapeutics

2021 ◽  
Vol 2 (2) ◽  
pp. 1-15
Author(s):  
Rehan Zafar Paracha ◽  
Fahed Parvaiz ◽  
Babar Aslam ◽  
Ayesha Obaid ◽  
Sidra Qureshi ◽  
...  
Keyword(s):  
Protein Interactions ◽  
Viral Protein ◽  
Influenza A ◽  
Viral Infections ◽  
Treatment Options ◽  
Interaction Network ◽  
Viral Proteins ◽  
Protein Protein Interactions ◽  
Virus Influenza

Viral infections are the cause of serious infirmities in humans and kill millions of people every year. Management of viral diseases is one of the challenges faced by the whole world which needs improvement in prevention and treatment options. Complete understanding of the consequences of viral proteins interaction network on host physiology is essential. Towards this goal, deciphering viral protein-protein interactions is one of the perspective which can help in our understanding about the basis of viral pathogenesis and the development of new antivirals. Indeed, viral infection network based on viral-viral proteins will provide an elusive and investigative framework to articulate rationalize drug discovery based on proteomics scale of viruses. In this study, proteomics a collection of viral-viral protein interactions reporting different studies of Hepatitis C virus, Influenza A virus, Dengue virus and SARS Coronavirus. Our effort of protein-interactions was focused on different studies reporting interactions between viral proteins encoded by the viruses under study. The study is integrated with a broad and original literature-curated data of viral-viral protein (197 non-redundant) interactions.

scholarly journals Tetraspanins: Host Factors in Viral Infections

2021 ◽  
Vol 22 (21) ◽  
pp. 11609
Author(s):  
ChihSheng New ◽  
Zhao-Yong Lee ◽  
Kai Sen Tan ◽  
Amanda Huee-Ping Wong ◽  
De Yun Wang ◽  
...  
Keyword(s):  
Influenza A ◽  
Viral Infections ◽  
Syncytium Formation ◽  
Life Cycles ◽  
Host Factors ◽  
Relative Contribution ◽  
Immunodeficiency Virus ◽  
Membrane Attachment ◽  
Compare And Contrast

Tetraspanins are transmembrane glycoproteins that have been shown increasing interest as host factors in infectious diseases. In particular, they were implicated in the pathogenesis of both non-enveloped (human papillomavirus (HPV)) and enveloped (human immunodeficiency virus (HIV), Zika, influenza A virus, (IAV), and coronavirus) viruses through multiple stages of infection, from the initial cell membrane attachment to the syncytium formation and viral particle release. However, the mechanisms by which different tetraspanins mediate their effects vary. This review aimed to compare and contrast the role of tetraspanins in the life cycles of HPV, HIV, Zika, IAV, and coronavirus viruses, which cause the most significant health and economic burdens to society. In doing so, a better understanding of the relative contribution of tetraspanins in virus infection will allow for a more targeted approach in the treatment of these diseases.

scholarly journals Switching Sides: How Endogenous RetrovirusesProtect us from Viral Infections

2021 ◽  
Author(s):  
Smitha Srinivasachar Badarinarayan ◽  
Daniel Sauter
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Dark Matter ◽  
Viral Infections ◽  
Endogenous Retroviruses ◽  
Viral Pathogens ◽  
Antiviral Immune Response ◽  
Cellular Immune ◽  
Antiviral Gene

Long disregarded as junk DNA or genomic dark matter, endogenous retroviruses (ERVs) turned out to represent important components of the antiviral immune response. These remnants of once-infectious retroviruses not only regulate cellular immune activation, but may even directly target invading viral pathogens. In this review, we summarize mechanisms, by which retroviral fossils protect us from viral infections. One focus will be on recent advances in the role of ERVs as regulators of antiviral gene expression.

Host-cell dependent role of phosphorylated keratin 8 during influenza A/NWS/33 virus (H1N1) infection in mammalian cells

2021 ◽  
Vol 295 ◽  
pp. 198333
Author(s):  
Flora De Conto ◽  
Francesca Conversano ◽  
Sergey V. Razin ◽  
Silvana Belletti ◽  
Maria Cristina Arcangeletti ◽  
...  
Keyword(s):  
Host Cell ◽  
Mammalian Cells ◽  
Influenza A ◽  
Virus H1n1 ◽  
H1n1 Infection ◽  
Keratin 8

scholarly journals PPAR Gamma and Viral Infections of the Brain

2021 ◽  
Vol 22 (16) ◽  
pp. 8876
Author(s):  
Pierre Layrolle ◽  
Pierre Payoux ◽  
Stéphane Chavanas
Keyword(s):  
Viral Infections ◽  
Ppar Gamma ◽  
Brain Parenchyma ◽  
Peroxisome Proliferator ◽  
Neural Cells ◽  
Peroxisome Proliferator Activated Receptor ◽  
Immunodeficiency Virus ◽  
Health And Disease ◽  
The Brain

Peroxisome Proliferator-Activated Receptor gamma (PPARγ) is a master regulator of metabolism, adipogenesis, inflammation and cell cycle, and it has been extensively studied in the brain in relation to inflammation or neurodegeneration. Little is known however about its role in viral infections of the brain parenchyma, although they represent the most frequent cause of encephalitis and are a major threat for the developing brain. Specific to viral infections is the ability to subvert signaling pathways of the host cell to ensure virus replication and spreading, as deleterious as the consequences may be for the host. In this respect, the pleiotropic role of PPARγ makes it a critical target of infection. This review aims to provide an update on the role of PPARγ in viral infections of the brain. Recent studies have highlighted the involvement of PPARγ in brain or neural cells infected by immunodeficiency virus 1, Zika virus, or human cytomegalovirus. They have provided a better understanding on PPARγ functions in the infected brain, and revealed that it can be a double-edged sword with respect to inflammation, viral replication, or neuronogenesis. They unraveled new roles of PPARγ in health and disease and could possibly help designing new therapeutic strategies.

scholarly journals Extracellular Vesicles in the Pathogenesis of Viral Infections in Humans

Viruses ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1200 ◽  
Author(s):  
Allen Caobi ◽  
Madhavan Nair ◽  
Andrea D. Raymond
Keyword(s):  
Extracellular Vesicles ◽  
Viral Infections ◽  
Membrane Vesicles ◽  
Response Modulation ◽  
Viral Spread ◽  
Neurotropic Viruses ◽  
Immunodeficiency Virus ◽  
Immune Response Modulation ◽  
Potential Use

Most cells can release extracellular vesicles (EVs), membrane vesicles containing various proteins, nucleic acids, enzymes, and signaling molecules. The exchange of EVs between cells facilitates intercellular communication, amplification of cellular responses, immune response modulation, and perhaps alterations in viral pathogenicity. EVs serve a dual role in inhibiting or enhancing viral infection and pathogenesis. This review examines the current literature on EVs to explore the complex role of EVs in the enhancement, inhibition, and potential use as a nanotherapeutic against clinically relevant viruses, focusing on neurotropic viruses: Zika virus (ZIKV) and human immunodeficiency virus (HIV). Overall, this review’s scope will elaborate on EV-based mechanisms, which impact viral pathogenicity, facilitate viral spread, and modulate antiviral immune responses.

Aids-Associated Viral Infections

1999 ◽  
Vol 5 (S2) ◽  
pp. 1098-1099
Author(s):  
Sara E. Miller
Keyword(s):  
Electron Microscopy ◽  
Human Immunodeficiency Virus ◽  
Viral Infections ◽  
Immune Defense ◽  
Detection Methods ◽  
Aids Patients ◽  
Viral Pathogens ◽  
Thin Sectioning ◽  
Immunodeficiency Virus ◽  
Life Threatening

Infection with human immunodeficiency virus (HIV) eventually causes a profound decrease in the body's ability to eradicate or control infections with microorganisms, including viruses. Some infections in AIDS patients are due to common organisms which are of little significance in immunocompetent individuals. Other organisms can be harbored continuously, occasionally causing disease, but normally being suppressed after a heightened immune defense; in AIDS patients, these infections can be life-threatening. Further, practices that predispose to HIV infection also permit entry of other organisms, such as hepatitis and herpesviruses. Electron microscopy is beneficial as an adjunct to other modalities for viral detection. Methods for identifying viruses, both in fluids by negative staining and in tissues by thin sectioning, have been published. Some viral pathogens, including HIV itself, are best documented by other means.HIV has been demonstrated by EM in infected individuals, but because it destroys and makes scarce the cells for which it has an affinity, it is difficult to find them.

scholarly journals Neutralization of Virus Infectivity by Antibodies: Old Problems in New Perspectives

2014 ◽  
Vol 2014 ◽  
pp. 1-24 ◽  
Author(s):  
P. J. Klasse
Keyword(s):  
Cellular Immunity ◽  
Neutralizing Antibodies ◽  
Viral Infections ◽  
Viral Proteins ◽  
Virus Neutralization ◽  
Virus Infectivity ◽  
Viral Pathogens ◽  
Enveloped Viruses ◽  
Vaccine Candidates ◽  
Hiv 1

Neutralizing antibodies (NAbs) can be both sufficient and necessary for protection against viral infections, although they sometimes act in concert with cellular immunity. Successful vaccines against viruses induce NAbs but vaccine candidates against some major viral pathogens, including HIV-1, have failed to induce potent and effective such responses. Theories of how antibodies neutralize virus infectivity have been formulated and experimentally tested since the 1930s; and controversies about the mechanistic and quantitative bases for neutralization have continually arisen. Soluble versions of native oligomeric viral proteins that mimic the functional targets of neutralizing antibodies now allow the measurement of the relevant affinities of NAbs. Thereby the neutralizing occupancies on virions can be estimated and related to the potency of the NAbs. Furthermore, the kinetics and stoichiometry of NAb binding can be compared with neutralizing efficacy. Recently, the fundamental discovery that the intracellular factor TRIM21 determines the degree of neutralization of adenovirus has provided new mechanistic and quantitative insights. Since TRIM21 resides in the cytoplasm, it would not affect the neutralization of enveloped viruses, but its range of activity against naked viruses will be important to uncover. These developments bring together the old problems of virus neutralization—mechanism, stoichiometry, kinetics, and efficacy—from surprising new angles.

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