Immunology: Human Sword against Viruses

Arnav Sinha
B.Tech Biotechnology
D.Y. Patil Biotechnology and Bioinformatics Institute

We live in a potentially hostile environment filled with a bewildering array of infectious agents that are always up for using us as rich sanctuaries for propagating their genes. In most instances, infection is resolved with or without tissue damage. The first vaccine development and administration that was devised by Edward Jenner in 1976 against small pox virus, paved ways for production of effective vaccines through these decades.

Classic examples include measles, mumps, rotavirus, rubella virus and varicella zoster viruses. Viruses such as HIV, hepatitis C (HCV), hepatitis B (HBV) and some herpes viruses can cause substantial tissue damage in most of the individuals they infect and their lesions can become chronic. Usually these viruses have one or more defying properties that allow them to diminish efficacy of host’s innate immunity for which we lack vaccines.

Infection with viruses such as influenza virus and respiratory syncytial virus (RSV) may cause mild to severe diseases that can be lethal. Of our particular interests are agents such as West Nile, dengue and polioviruses capable of causing overt diseases but in a minority of infected individuals. The level of concern increases for human T – Lymphotropic virus, Epstein-Barr virus (EBV) and possibly rubella virus as they are thought to act as triggering agents for autoimmune diseases and cancer in genetically susceptible individuals.

Ingress of almost all viruses cause recruitment and activation of inflammatory cell types particularly neutrophils and macrophages that in succession release a range of molecules like cytotoxic cytokines, cationic proteins and lipid mediators induce tissue damage or malfunction.

I was intrigued to learn about the presence of innate immune receptors which upon activation succours production of pro inflammatory cytokines, interferons and signals that recruit and activate the cells involved in inflammation and induction of adaptive immunity. The pattern of immune events induced after entry of virus dictates the outcome of infection in an individual.

Many viruses that persist trigger innate cells such as dendritic cells (DC), natural killer cells (NK) and macrophages to produce anti-inflammatory molecules such as interleukin-10 transforming growth factor β. DC from lymphocytic choriomeningitis virus (LCMV) infected mice produce high levels of IL-10 that is produced by monocytes from individuals infected with HIV, HCV or HBV. T-cells directly destroy virus infected cells or release cytokines such as tumour necrosis factor (TNF) that damage cells. Destruction of infected cells by effector T-cells is the main cause of liver damage in case of noncytopathic virus infections like HCV and HBV. Antibody response to viruses may also contribute to tissue damage like nephritis, polyarteritis and arthritis. Despite these occurrences, tissue damage is modest in most viral infections. The level of tissue damage can vary among individuals infected by
same virus. Whether a virus causes severe tissue damage often depends on age at which infections occur. In general it is the young and elderly who suffer most severe consequences of infections. The following table shows the virus and host features that favour tissue damage.

Feature Virus Effect on host
Interference with innate immune responses  




HCV Blocks RIG-1 pathway by degrading ips1
Influenza A virus NS1 protein inhibits RIG-1 by direct interaction
Interference with antigen processing and presentation  




HSV ICP47 blocks TAP-mediated peptide transport
HIV Nef protein inhibits cell surface expression of CD4 molecules
Dose of infection
High HBV Immunopathology of liver
Low LCMV Choriomeningitis
Host genetic susceptibility
Defective type 1 and 2 IFNs Poliovirus Increased susceptibility to paralysis
HSV Increased susceptibility to encephalitis
Age of infection


Influenza virus

and        RSV

Increased susceptibility to infection
Adult HSV Increased susceptibility to infection
Old Influenza virus

and     RSV

Increased susceptibility to infection

Mechanisms that determine the events following a viral infection involve the signaling mechanism of both innate and adaptive immune systems as for instance the impaired ability of effector T-cells to execute immune response can lead to an overt viral infection in the body, so the proper functioning of
both the arms of immune system along with the general physical wellbeing of an individual plays a vital role in determining the occurrence and severity of the infection. Numerous studies and researches have well established the importance of fully functional immune system in human health and disease so I would personally like to applaud the hard work and diligence of researchers improving our understanding in field of immunology.

Reference (Dec-20-A7)

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