Rapid Communication - Virology Research Journal (2023) Volume 7, Issue 2

Intricacies of virus-cell interactions and molecular interplay between viruses and host cells

Weber Nara^*

Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, United States

Corresponding Author:

Weber Nara
Department of Biomedical Sciences
College of Veterinary Medicine
Cornell University, Ithaca
NY 14853, United States
E-mail: weber@cornell.edu

Received: 24-Feb-2023, Manuscript No. AAVRJ-23-90740; Editor assigned: 25-Feb-2023, PreQC No. AAVRJ-23-90740(PQ); Reviewed: 10-Mar-2023, QC No. AAVRJ-23-90740; Revised: 15-Mar-2023, Manuscript No. AAVRJ-23-90740(R); Published: 21-Mar-2023, DOI:10.35841/AAVRJ-7.2.138

Citation: Nara W. Intricacies of virus-cell interactions and molecular interplay between viruses and host cells. Virol Res J. 2023;7(2):138

Introduction

Viruses are obligate intracellular parasites that cannot replicate outside their host cells. To complete their life cycle, they need to enter host cells, hijack the host cellular machinery, and use it for their own replication. However, this process is not as simple as it seems, as the interaction between viruses and host cells is complex and intricate. In this essay, we will explore the intricacies of virus-cell interactions and the molecular interplay between viruses and host cells.

Virus Entry into Host Cells

The first step of virus-cell interaction is the entry of the virus into the host cell. The mechanisms of virus entry can vary among different viruses, and they often depend on the type of host cell and the specific receptors present on its surface. Some viruses, such as influenza virus, enter host cells by receptormediated endocytosis. The virus binds to specific receptors on the cell surface, which triggers the formation of a vesicle that engulfs the virus particle and pulls it into the cell. Once inside the cell, the virus must uncoat its genetic material and release it into the host cell cytoplasm to initiate replication. Other viruses, such as HIV, use a different mechanism of entry. They interact with specific receptors on the cell surface and then fuse their envelope with the cell membrane, releasing their genetic material directly into the host cell cytoplasm [1].

Virus Replication in Host Cells

Once the virus enters the host cell, it must replicate its genetic material and produce new virus particles. The replication of viruses is dependent on the host cell machinery, as viruses lack the ability to replicate independently [2-5]. The replication of RNA viruses, such as the common cold virus, involves the synthesis of a complementary RNA strand using the host cell machinery. This complementary RNA strand serves as a template for the synthesis of new virus RNA strands.

DNA viruses, such as herpes simplex virus, use a different strategy. They integrate their genetic material into the host cell DNA and use the host cell machinery to replicate their DNA.

Molecular Interplay between Viruses and Host Cells

The interaction between viruses and host cells is a complex interplay between viral and host cell molecules. Viruses must evade the host cell immune system to successfully replicate, and they do this by exploiting various mechanisms that enable them to evade detection by the immune system.

One mechanism that viruses use to evade the immune system is the production of proteins that interfere with the host cell's antiviral response. For example, HIV produces a protein called Vif that inhibits the host cell's ability to restrict viral replication by targeting viral RNA for destruction. Another mechanism that viruses use to evade the immune system is the modification of their surface proteins to evade detection by the host cell immune system. Influenza virus, for example, modifies its surface proteins to avoid detection by antibodies produced by the host cell immune system.

In addition to evading the host cell immune system, viruses also manipulate host cell signaling pathways to promote their replication. For example, the Ebola virus produces a protein called VP35, which inhibits the host cell's ability to produce interferons, signaling molecules that activate the host cell's immune response.

Conclusion

In summary, the interaction between viruses and host cells is a complex and intricate process that involves the entry of the virus into the host cell, the replication of the virus within the host cell, and the molecular interplay between the virus and the host cell. Viruses must evade the host cell immune system and manipulate host cell signaling pathways to successfully replicate. Understanding the intricacies of virus-cell interactions and the molecular interplay between viruses and host cells is crucial for the development of effective antiviral therapies and vaccines.

References

1. Nickol ME, Kindrachuk J. Dysregulated Host Responses Underlie 2009 Pandemic Influenza-Methicillin Resistant Staphylococcus aureus Coinfection Pathogenesis at the Alveolar-Capillary Barrier. Cells. 2020;9(11):2472.

Indexed at, Google Scholar, Cross Ref

2. Paparisto E, Hunt NR. Interferon-Induced HERC5 Inhibits Ebola Virus Particle Production and Is Antagonized by Ebola Glycoprotein. Cells. 2021;10(9):2399.

Indexed at, Google Scholar, Cross Ref

3. Courtney DG. Post-Transcriptional Regulation of Viral RNA through Epitranscriptional Modification. Cells. 2021;10(5):1129.

Indexed at, Google Scholar, Cross Ref

4. Xue L, Weilong J. Coinfection of Porcine Circovirus 2 and Pseudorabies Virus Enhances Immunosuppression and Inflammation through NF-κB, JAK/STAT, MAPK, and NLRP3 Pathwaysn. Int J Mol Sci. 2022;23(8):4469

Indexed at, Google Scholar, Cross Ref

5. Chailangkarn T, Tanwattana N. Establishment of Human-Induced Pluripotent Stem Cell-Derived Neurons-A Promising In Vitro Model for a Molecular Study of Rabies Virus and Host Interaction. Int J Mol Sci 2021;22(21):11986.
Indexed at, Google Scholar, Cross Ref