Rapid Communication - Virology Research Journal (2023) Volume 7, Issue 3

Targeting viral evasion strategies for antiviral development and host immune responses

Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA

*Corresponding Author:

Mbamalu ON
Department of Microbiology
Immunology, and Molecular Genetics
University of California, Los Angeles
Los Angeles, CA 90095, USA
E-mail: chou@mednet.ucla.edu

Received: 21-Apr-2023, Manuscript No. AAVRJ-23-97699; Editor assigned: 22-Apr-2023, PreQC No. AAVRJ-23-97699(PQ); Reviewed: 06-May-2023, QC No. AAVRJ-23-97699; Revised: 13-May-2023, Manuscript No. AAVRJ-23-97699(R); Published: 20-May-2023, DOI:10.35841/AAVRJ-7.3.145

Citation: Chen C. Targeting viral evasion strategies for antiviral development and host immune responses. Virol Res J. 2023;7(3):145

Introduction

Viral infections are a significant threat to human health, with viruses such as HIV, hepatitis B and C, influenza, and Zika virus causing significant morbidity and mortality worldwide. Antiviral therapy is one of the primary strategies for managing viral infections, but the development of resistance to these drugs is a significant challenge. One reason for this is that viruses have evolved multiple strategies to evade the host immune response and antiviral therapy. Targeting these viral evasion strategies may provide new opportunities for antiviral development and improve host immune responses. Viruses have evolved multiple strategies to evade or subvert the host immune response, allowing them to establish chronic infections and persist in the host. These strategies include antigenic variation, suppression of immune responses, hiding from the immune system, and production of decoy molecules. Antigenic variation is a common viral evasion strategy, where viruses mutate rapidly, leading to the production of new viral variants that are not recognized by the host immune system. For example, HIV has a high mutation rate, which allows it to escape recognition by the immune system and persist in the host. Suppression of immune responses is another viral evasion strategy, where viruses produce proteins that can inhibit the function of immune cells, such as T cells and dendritic cells. For example, hepatitis C virus produces a protein called NS5A that can inhibit the production of interferon, a cytokine that plays a critical role in the immune response to viral infections [1].

Viruses can also hide from the immune system by infecting immune cells themselves. For example, HIV can infect CD4+ T cells, which are critical immune cells that play a central role in the adaptive immune response. By infecting these cells, the virus can avoid detection by the immune system and establish a persistent infection. Another viral evasion strategy is the production of decoy molecules that can bind to and neutralize antibodies. For example, herpesviruses produce glycoproteins that can bind to antibodies and prevent them from neutralizing the virus. This allows the virus to persist in the host and cause recurrent infections [2].

Targeting viral evasion strategies provides new opportunities for antiviral development and improving host immune responses. By disrupting viral evasion strategies, antiviral therapy can enhance the host immune response and increase the effectiveness of antiviral drugs. One approach is to target viral proteins or enzymes that are essential for viral replication or immune evasion. For example, direct-acting antivirals (DAAs) for hepatitis C virus target viral enzymes such as the NS3/4A protease and the NS5B RNA polymerase. These drugs have revolutionized the treatment of hepatitis C, with cure rates exceeding 95% in some populations. Another approach is to target viral proteins that interact with the host immune system, such as immune checkpoint inhibitors. Immune checkpoints are molecules that regulate immune responses to prevent overactivation and tissue damage. However, some viruses can exploit these checkpoints to suppress the immune response. Immune checkpoint inhibitors are drugs that can block these checkpoints, allowing the immune system to mount a more robust response to viral infections.Gene-editing technologies, such as CRISPR/Cas9, provide another approach to targeting viral evasion strategies. These technologies can target viral DNA and eliminate infected cells, preventing the virus from replicating and establishing chronic infections. Preclinical studies have shown promise for the use of gene editing in the treatment of chronic viral infections, such as HIV and hepatitis B. Targeting viral evasion strategies can also improve host immune responses, enhancing the ability of the host immune system to recognize and eliminate viral infections. For example, immune checkpoint inhibitors can block the suppression of T cell function by viruses, enhancing the ability of the immune system to eliminate infected cells. Similarly, vaccines can be designed to target viral evasion strategies, improving the effectiveness of vaccination and reducing the risk of infection [3].

One promising strategy is to design vaccines that target conserved regions of viral proteins that are less likely to mutate and evade the immune response. For example, the influenza virus vaccine targets the hemagglutinin and neuraminidase proteins, which are critical for viral entry and exit, respectively. These proteins are highly conserved among influenza viruses, allowing the vaccine to provide broad protection against different strains of the virus. Another approach is to design vaccines that stimulate both the innate and adaptive immune systems. Innate immune responses are the first line of defense against viral infections and can help to shape the adaptive immune response. For example, the use of adjuvants, such as aluminum salts, can stimulate the innate immune system and enhance the effectiveness of vaccines. Finally, targeting viral evasion strategies can also provide new opportunities for developing immunotherapies for viral infections. For example, chimeric antigen receptor (CAR) T cell therapy, which involves engineering T cells to express CARs that target viral antigens, has shown promise in preclinical studies of chronic viral infections, such as HIV.

In conclusion, targeting viral evasion strategies provides new opportunities for antiviral development and improving host immune responses. Viruses have evolved multiple strategies to evade or subvert the host immune response, allowing them to establish chronic infections and persist in the host. By disrupting viral evasion strategies, antiviral therapy can enhance the host immune response and increase the effectiveness of antiviral drugs. Targeting viral evasion strategies can also improve host immune responses, enhancing the ability of the host immune system to recognize and eliminate viral infections. These strategies have the potential to revolutionize the treatment and prevention of viral infections, improving the health outcomes of millions of people worldwide [4,5].

References

1. Linnekamp JF. Clinical and biological effects of demethylating agents on solid tumours – a systematic review. Cancer Treat Rev. 2017;54:10-23.

Indexed at, Google Scholar, Cross Ref

2. Qiu Z.  ATR/CHK1 inhibitors and cancer therapy Radiother. Oncol. 2018;126: 450-64.

Indexed at, Google Scholar, Cross Ref

3. Nanbo A. Epstein–Barr virus RNA confers resistance to interferon-α-induced apoptosis in Burkitt's lymphoma.EMBO J. 2002; 21;954-65.

Indexed at, Google Scholar, Cross Ref

4. Arrand JR. Two families of sequences in the small RNA-encoding region of Epstein-Barr virus (EBV) correlate with EBV types A and B. J.Virol. 1989; 63:983-6.

Indexed at, Google Scholar, Cross Ref

5. West JA, Wicks M. An important role for mitochondrial antiviral signaling protein in the Kaposi's sarcoma-associated herpesvirus life cycle. J. Virol. 2014; 88: 5778-87.

Indexed at, Google Scholar, Cross Ref