Essay on Viruses and Immune System

Viruses are small, obligate intracellular parasites which cause infection by invading cells of the body and multiplying within them. Within their life cycle they have a relatively short extracellular period, prior to infecting the cells, and a longer intracellular period during which they undergo replication.

The immune system has mechanisms which can attack the virus in both these phases of its life cycle, and this involves both non-specific and specific effectors mechanisms.

Non-Specific Mechanisms

Interferons:

Viral infection of cells directly stimulates the production of Type I interferons. Type I interferon’s lead to the induction of an “antiviral state” in the cells that is characterized by inhibition of both viral replication and cell proliferation, and also enhancement of the ability of natural killer cells to lyse virally infected cells.

Natural Killer Cells:

Natural killer (NK) cells lyse virally infected cells. Even though they are not antigen specific, they clearly exhibit some degree of selectivity in targeting “abnormal” cells for lysis.

Thus NK cells may be effective early in the course of viral infection, and may limit the spread of infection during the early stage, while antigen-specific lymphocytes are being recruited and clonally expanded.

Specific Mechanisms

Both humoral and cell mediated arms of the immune response play a role as specific effector mechanisms in antiviral immunity.

Antibody:

Specific antibodies are important in defence mechanism to provide protection against viral infections. The most effective type of antiviral antibody is “neutralizing” antibody – this antibody binds to the virus (usually to the viral envelope), and blocks the virus from binding and gaining entry in to the host cell. It also acts as opsonin in enhancing phagocytosis of virus particles.

Cytotoxic T Cells:

The principal effector cells which are involved in clearing established viral infections are the virus specific CD₈ ⁺ cytotoxic T lymphocytes (CTL). These cells recognise (viral) antigens which have been synthesised within cell’s nucleus or cytosol, and which have been degraded.

Although the host has a variety of defenses to protect against viral infections, sometimes it is the immune response to the infection that is the direct cause of tissue injury. For example, infants infected with cytomegalovirus have circulating immune complexes that are deposited in the kidneys and joints resulting in pathology such as arthritis and glomerular nephritis.

Viruses have evolved a variety of strategies to evade immune recognition and persist unmolested in the host. Many viruses are able to suppress immune responses and thereby overcome or minimize host defenses. The evasion of virus is accomplished by several mechanisms. They are as follows:

Antigenic drift and shift:

Viruses show an antigenic drift, as mutation and selection gradually change the aminoacid sequence of the surface antigens. For example Influenza virus in human population shows great antigenic variation within each subtype.

This permits the parasite to persist in a population for many years. The antigenic shift in Influenza virus results in development of new strains.

Rapid turnover:

The rapid turn over of population ensures the persistence of Influenza virus with out antigenic drift in horse.

Antigen presentation:

Viral interference with antigen presentation via MHC class I is observed during infection with numerous viruses and is interpreted as a mechanism for viral escape from cytotoxic T (Tc) cell recognition. Interference is exerted at diverse stages of the MHC class I antigen processing and presentation pathway.

Inhibition of apoptosis:

The phosphatidylinositol 3-kinase (PI3K) – Akt pathway is utilized by many cell types for inhibition of apoptosis and cellular survival. Virus modulation of this pathway provides an alternative to the expression of viral oncogenes or the direct inhibition of pro-apoptotic proteins.

Inability of host antibodies to neutralize virus:

The best example is HIV which infects the CD₄ ⁺ cells thereby destroying the specific immune system. Other viruses for eg. measles virus can also infect lymphocytes and affect their replication and differentiation.