Special Issue "Host Cell-Virus Interaction"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editors

Dr. Parikshit Bagchi
E-Mail Website
Guest Editor
Cell and Developemental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Interests: Host cell-virus interaction; intracellular trafficking of virus; membrane trafficking; non-enveloped viruses; positive sense RNA viruses
Dr. Anupam Mukherjee
E-Mail Website
Guest Editor
ICMR-National AIDS Research Institute
Interests: RNA virus; Viral pathogenesis; Host cell-virus interaction; RNAi; Small RNA as theraputics; Targated delivery; Virus & Cancer

Special Issue Information

Dear Colleagues,

Every virus needs to hijack a host cell, be it a plant, animal, insect, or even a bacterial cell, to replicate and survive at the cost of its host. It is the interactions of the virus with the host cell that holds the deepest and darkest secrets of the virus, the unravelling of which opens multiple avenues in anti-viral research. The study of host cell-virus interaction not only provides important information about virus pathogenesis; it also often has great importance in other fields of research, especially in the field of cell biology and immunology. There are several instances where novel cellular functions of a host protein were revealed by studying host cell-virus interaction. This valuable information can go a long way in understanding interactions with other related viruses as well. The regulation of cellular immune responses is another significant component of viral pathogenesis. Important knowledge regarding immunological modulation after viral infection can help to establish strategies to fight against viral infection. In this special issue, we will focus on studies related to the exploitation of host cells by viruses for successful infection, and will highlight the counteractive host cell measures employed in order to win the war against the viruses.

Dr. Parikshit Bagchi
Dr. Anupam Mukherjee
Guest Editors

Manuscript Submission Information

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Keywords

  • virus
  • host cell
  • host-virus interaction
  • virus entry
  • virus assembly and egress
  • viral replication and pathogenesis
  • viral immune evasion
  • anti-viral strategies
  • intracellular trafficking of virus

Published Papers (2 papers)

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Research

Article
HTLV-2 Encoded Antisense Protein APH-2 Suppresses HIV-1 Replication
Viruses 2021, 13(8), 1432; https://doi.org/10.3390/v13081432 - 23 Jul 2021
Viewed by 469
Abstract
Antisense protein of Human T-cell Leukemia Virus Type 2 (HTLV-2), also called APH-2, negatively regulates the HTLV-2 and helps the virus to maintain latency via scheming the transcription. Despite the remarkable occurrence of HTLV-2/HIV-1 co-infection, the role of APH-2 influencing HIV-1 replication kinetics [...] Read more.
Antisense protein of Human T-cell Leukemia Virus Type 2 (HTLV-2), also called APH-2, negatively regulates the HTLV-2 and helps the virus to maintain latency via scheming the transcription. Despite the remarkable occurrence of HTLV-2/HIV-1 co-infection, the role of APH-2 influencing HIV-1 replication kinetics is poorly understood and needs investigation. In this study, we investigated the plausible role of APH-2 regulating HIV-1 replication. Herein, we report that the overexpression of APH-2 not only hampered the release of HIV-1 pNL4.3 from 293T cells in a dose-dependent manner but also affected the cellular gag expression. A similar and consistent effect of APH-2 overexpression was also observed in case of HIV-1 gag expression vector HXB2 pGag-EGFP. APH-2 overexpression also inhibited the ability of HIV-1 Tat to transactivate the HIV-1 LTR-driven expression of luciferase. Furthermore, the introduction of mutations in the IXXLL motif at the N-terminal domain of APH-2 reverted the inhibitory effect on HIV-1 Tat-mediated transcription, suggesting the possible role of this motif towards the downregulation of Tat-mediated transactivation. Overall, these findings indicate that the HTLV-2 APH-2 may affect the HIV-1 replication at multiple levels by (a) inhibiting the Tat-mediated transactivation and (b) hampering the virus release by affecting the cellular gag expression. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction)
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Article
Viperin, an IFN-Stimulated Protein, Delays Rotavirus Release by Inhibiting Non-Structural Protein 4 (NSP4)-Induced Intrinsic Apoptosis
Viruses 2021, 13(7), 1324; https://doi.org/10.3390/v13071324 - 08 Jul 2021
Viewed by 571
Abstract
Viral infections lead to expeditious activation of the host’s innate immune responses, most importantly the interferon (IFN) response, which manifests a network of interferon-stimulated genes (ISGs) that constrain escalating virus replication by fashioning an ill-disposed environment. Interestingly, most viruses, including rotavirus, have evolved [...] Read more.
Viral infections lead to expeditious activation of the host’s innate immune responses, most importantly the interferon (IFN) response, which manifests a network of interferon-stimulated genes (ISGs) that constrain escalating virus replication by fashioning an ill-disposed environment. Interestingly, most viruses, including rotavirus, have evolved numerous strategies to evade or subvert host immune responses to establish successful infection. Several studies have documented the induction of ISGs during rotavirus infection. In this study, we evaluated the induction and antiviral potential of viperin, an ISG, during rotavirus infection. We observed that rotavirus infection, in a stain independent manner, resulted in progressive upregulation of viperin at increasing time points post-infection. Knockdown of viperin had no significant consequence on the production of total infectious virus particles. Interestingly, substantial escalation in progeny virus release was observed upon viperin knockdown, suggesting the antagonistic role of viperin in rotavirus release. Subsequent studies unveiled that RV-NSP4 triggered relocalization of viperin from the ER, the normal residence of viperin, to mitochondria during infection. Furthermore, mitochondrial translocation of NSP4 was found to be impeded by viperin, leading to abridged cytosolic release of Cyt c and subsequent inhibition of intrinsic apoptosis. Additionally, co-immunoprecipitation studies revealed that viperin associated with NSP4 through regions including both its radical SAM domain and its C-terminal domain. Collectively, the present study demonstrated the role of viperin in restricting rotavirus egress from infected host cells by modulating NSP4 mediated apoptosis, highlighting a novel mechanism behind viperin’s antiviral action in addition to the intricacy of viperin–virus interaction. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction)
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