Short Communication - Virology Research Journal (2023) Volume 7, Issue 3
Host-virus interactions in viral replication and their strategies and mechanismsCristinia Zhou*
Department of Microbiology, Faculty of Naval Medicine, Naval Medical University, Shanghai 200433, China
- *Corresponding Author:
- Cristinia Zhou
Department of Microbiology
Faculty of Naval Medicine
Naval Medical University
Shanghai 200433, China
Received: 19-Apr-2023, Manuscript No. AAVRJ-23-97698; Editor assigned: 20-Apr-2023, PreQC No. AAVRJ-23-97698(PQ); Reviewed: 04-May-2023, QC No. AAVRJ-23-97698; Revised: 11-May-2023, Manuscript No. AAVRJ-23-97698(R); Published: 18-May-2023, DOI:10.35841/AAVRJ-7.3.144
Citation: Zhou C. Host-virus interactions in viral replication and their strategies and mechanisms. Virol Res J. 2023;7(3):144
Viruses are obligate intracellular parasites that depend on host cells for replication and propagation. Host-virus interactions play a crucial role in viral replication and can determine the outcome of viral infections. Viruses have evolved various strategies and mechanisms to interact with host cells and exploit their resources for replication. In this article, we will explore the host-virus interactions in viral replication, their strategies, and mechanisms.
The first step in viral replication is the entry of the virus into host cells. Viruses use various mechanisms to enter host cells, such as receptor-mediated endocytosis, membrane fusion, and direct penetration. Some viruses use specific receptors on host cells to enter, such as the human immunodeficiency virus (HIV), which uses the CD4 receptor and co-receptors to enter immune cells. Other viruses, such as the influenza virus, use a receptor-mediated endocytosis mechanism to enter host cells. Once the virus enters the host cell, it must recognize and attach to specific host cell receptors to initiate viral replication . Host cells express various receptors on their surfaces that viruses can use to attach and enter cells. For example, the severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) uses the angiotensin-converting enzyme 2 (ACE2) receptor to enter host cells. The attachment of the virus to the host cell receptor triggers conformational changes in the virus that allow it to enter the host cell.
After entering the host cell, the virus uses host cell machinery to replicate its genome and synthesize viral proteins. Viruses have evolved various strategies to evade the host cell's immune response and replicate efficiently . For example, some viruses encode proteins that interfere with host cell gene expression, suppress host cell antiviral responses, or modulate host cell signaling pathways to facilitate viral replication. During the replication process, viruses can induce various changes in host cells, such as inducing apoptosis or triggering immune responses. Some viruses have evolved mechanisms to evade host cell immune responses, such as the human papillomavirus (HPV), which can suppress host cell immune responses by inhibiting the expression of interferon-stimulated genes. Viral assembly is the process by which newly synthesized viral components are assembled into mature virions. Viruses use host cell resources and machinery to assemble new virions. For example, the HIV virus uses host cell membranes and the host cell's endoplasmic reticulum to assemble new virions. The final step in viral replication is the release of mature virions from the host cell and transmission to new host cells. Viruses use various mechanisms to exit host cells, such as budding, lysis, and exocytosis. Some viruses can also modulate host cell signaling pathways to facilitate viral exit, such as the hepatitis C virus (HCV), which can induce lipid droplet formation in host cells, facilitating viral assembly and exit. Viruses have evolved various strategies and mechanisms to interact with host cells and exploit their resources for replication. Some of the common strategies and mechanisms include:
Viruses can evade the host immune response by interfering with host cell signaling pathways, inhibiting host cell antiviral responses, or modulating host cell gene expression. For example, the human cytomegalovirus (HCMV) can suppress host cell antiviral responses by inhibiting the expression of interferon-stimulated genes.
Viruses can modulate host cell cycle checkpoints to promote viral replication and avoid host cell apoptosis. For example, the human papillomavirus (HPV) can induce host cell proliferation and suppress apoptosis, promoting viral replication and persistence . Viruses can ensure efficient replication and transmission by maintaining high replication fidelity and avoiding errors that can lead to the production of non-functional virions. Viruses use various mechanisms to maintain replication fidelity, such as proofreading and error correction mechanisms. For example, the HIV virus encodes a reverse transcriptase enzyme with proofreading activity, which helps maintain high replication fidelity [4,5].
Some viruses can integrate their genome into the host cell genome, allowing the virus to persist and replicate over a long period. For example, the human immunodeficiency virus (HIV) can integrate its genome into the host cell genome, leading to persistent viral infection. Some viruses can establish a latent state in host cells, where the virus remains dormant for long periods without replicating. For example, the herpes simplex virus (HSV) can establish a latent infection in neurons, where the virus remains dormant until reactivation, leading to recurrent infections.
Host-virus interactions play a crucial role in viral replication, and viruses have evolved various strategies and mechanisms to interact with host cells and exploit their resources for replication. Understanding the mechanisms of host- virus interactions can help in the development of antiviral therapies and vaccines that target specific viral strategies and mechanisms. Antiviral therapies can target viral entry, replication, assembly, and exit, while vaccines can induce host cell immunity against viral infection. Future research in host- virus interactions can lead to the development of more effective antiviral therapies and vaccines to combat viral infections.
- Xie Y TZ, Qu YC. Expression and clinical value of serum microRNA-143 in HBV associated liver diseases. Chin J Clin (Electron Ed). 2013;7:11370-75.
- Winther TN. Differential plasma microRNA profiles in HBeAg positive and HBeAg negative children with chronic hepatitis B. PLoS One. 2013;8:e58236.
- Wei YF, Cui GY. MicroRNAs may solve the mystery of chronic hepatitis B virus infection. World J Gastroenterol. 2013;19:4867-76.
- Wang XW, Orum H. MicroRNAs in liver disease. Gastroenterology. 2012; 142:1431-43.
- Coulouarn C. Loss of miR-122 expression in liver cancer correlates with suppression of the hepatic phenotype and gain of metastatic properties. Oncogene. 2009;28:3526-36.