Virus Prevention and Treatment

Host Immunity to Virus Infections

An individual is exposed to many infectious agents, however, in most situations does not develop a disease thanks to factors such as physical and chemical host barriers. If the virus is able to overcome these first lines of defense, a type of highly specialized and specific protection will be activated. This defense will achieve, in most situations, the infection control and subsequent eradication of the disease.

• Innate immunity

Innate immune defense provides the first line against viral infections. The innate immune system is composed mainly of physical barriers, chemical barriers, innate immune cells, and soluble mediators such as the complement system, innate antibodies, and associated cytokines. The cells mediating innate immunity do not respond to specific viral antigens as do their counterparts in the adaptive immune response. Several distinct activities mediate innate immune defense against viruses, including:

• Epithelial barriers. Anatomic barriers, secretions, and other activities at mucosal surfaces provide non-specific protection against viral infection.
• Interferon (IFN) responses. IFN are key elements of antiviral resistance at the cellular level. They play a central role in both innate and adaptive immune responses to viral infections.
• Natural killer (NK) cells can recognize host cells that express altered levels of major histocompatibility complex (MHC) class I molecules and/or heat shock (or similar) proteins or bind antibody-coated target cells to mediate death of virus-infected cells via lysis and apoptosis.
• The activities of phagocytic cells such as neutrophils, macrophages, and dendritic cells. Phagocytic cells have a direct role in limiting viral spread by phagocytosis of apoptotic infected cells and by phagocyte-mediated opsonophagocytosis of virus particles.
• Gene Silencing: small RNA molecules that interfere with virus replication (RNAi).

• Adaptive immunity
• Humoral Immunity. B lymphocytes produce antibodies that are responsible for, amongst other activities, neutralization, and clearance of cell-free viruses. Antibodies also mediate long-term protection against reinfection by many viruses.
• Cellular Immunity including virus-specific CD4+ T cells and CD8+ T cells.

The killing of virus-infected cells by cytotoxic T lymphocytes (CD8+ T cells) is achieved by the release of cytotoxic granules at the interface between the receptor-bound T cell and a virus-infected cell including perforin, granzymes, and granulysin. Cytotoxic CD8 T cells can also release cytokines that act either locally or at a distance to impact virus infection, such as IFN-γ, which can block virus replication and even eliminate the virus from infected cells without inducing cell death.

A key function of effector CD4 T cells is to provide help to CD8 T cells, an essential step in the activation of cytotoxic T lymphocytes in the majority of viral infections. In addition to the helper function, CD4+ T cells also display cytolytic activity.

Fig.1 Induction of humoral and cellular immunity in the viral infection. (Van de Sandt, 2012)

Virus Prevention and Treatment

Each virus can cause different cytopathic effects in the host cell, which may lead to several symptoms and disease. There are some strategies against viral infections:

• Vaccination. Vaccination is the most effective way of preventing viral diseases. Except for living virus vaccines, the second era of vaccination is introduced, and many live-attenuated virus and inactivated virus vaccines are developed. More recently, the field of vaccinology has witnessed the introduction of a number of novel “new generation” vaccines produced through various forms of recombinant DNA and related technologies.
• Anti-viral agents. Anti-viral agents may be to prevent virus infection or replication at mucosal surfaces and prevent epithelial damage, inflammation, mucous production, activation of macrophages, and attraction of neutrophils. Some anti-virus drug interaction sites include polymerase inhibitors, (nucleoside) reverse transcriptase inhibitors, RNA polymerase inhibitors including nonstructural protein 5 inhibitors (NS5A) and NS5B inhibitors, protease inhibitors, integrase inhibitors, entry inhibitors, and neuraminidase inhibitors. In addition, virus-specific antibodies have been licensed for use in anti-virus infections.

Fig.2 The viral life cycle and drug interaction sites. (Slagman, 2021)

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References

1. Van de Sandt, C.E.; et al. Evasion of influenza A viruses from innate and adaptive immune responses. Viruses. 2012, 4(9): 1438-76.
2. Slagman,S.; Fessner, W.D. Biocatalytic routes to anti-viral agents and their synthetic intermediates. Chem Soc Rev. 2021. 50(3): 1968-2009.

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