Viruses are well known for stimulating innate immune responses. Certain viruses, in particular, induce the production of interferons, which can inhibit viral replication by causing an antiviral reaction. NK cells are also in charge of virus control. NK cells are often the first line of protection against viral infections. To eliminate an infectious virus, a number of immune effector functions, as well as non-unique defense mechanisms, are activated. Simultaneously, the virus acts to destabilize one or all of these channels in order to prolong its own life.
The innate immune response to viral infection is mainly mediated by the recruitment of type I interferons (IFN- and IFN-) and the activation of NK cells. Double stranded RNA (dsRNA) produced during the viral life cycle can cause the development of IFN- and IFN- by infected cells. Macrophages, monocytes, and fibroblasts may also synthesize these cytokines, but the mechanisms in these cells that lead to the production of type I interferons remain unknown. By binding to the α / β-IFN receptor, IFN-α and IFN-β can induce an antiviral reaction or viral replication resistance. When bound, the JAK-STAT pathway is activated by IFN-α and IFN-β, resulting in the transcription of many genes.
Mechanisms of Humoral and Cell-Mediated Immune Responses to Viruses
Virus Neutralizing Antibodies
Antibodies unique to viral surface antigens are also critical when it comes to preventing the dissemination of a virus during acute infection and defending against infection when you are situated at the viral entry point. Most viruses express face receptor molecules that enable them to attach to different host-cell membrane molecules to initiate infection. So, e.g. Influenza virus binds to residues of sialic acid in cell membrane glycoproteins and glycolipids, and the Epstein-Bar virus binds B cells to type 2 complement receptors. If an antibody is produced to viral receptors, it can block infection altogether by preventing host cells from binding viral particles.
Antibody viral neutralization often includes pathways that act on host cells after viral attachment. In some cases, antibodies may block viral penetration by binding to epitopes needed to mediate viral envelope fusion with plasma membrane. If the mediated antibody is of a complement-activating isotype, it may result in lysis of enveloped virions.
Cell-Mediated Immunity in Viral Control and Clearance
While antibodies play an important role in preventing the spread of a virus in the acute phases of infection, they typically can not eradicate the virus once infection has occurred — especially if the virus is capable of reaching a latent state in which its DNA is incorporated into host chromosome DNA. The cell-mediated immune mechanisms are most effective in host protection once an infection is identified. CD8 + TC cells and CD4 + TH1 cells are usually the key components of cell-mediated antiviral resistance, while CD4 + TC cells have also been implicated in certain instances.
Activated TH1 cells release a variety of cytokines, including IL-2, IFN-ÿ and TNF, which either directly or indirectly protect against viruses. IFN-ÿ works specifically by causing an antiviral cell state. IL-2 functions implicitly by helping to integrate precursor CTL into an effector group. Both IL-2 and IFN-ÿ activate NK cells, which during the first days of many viral infections play an important role in host defense until a specific CTL response develops.
Relevant CTL activity in most viral infections occurs within 3–4 days after infection, increases 7–10 days after infection and then decreases. Some virions were removed within 7–10 days of primary infection, parallel to the growth of the CTLs. The virus-specific CTLs kill virus-infected self-cells and thereby remove possible new virus origins. The role of CTLs in virus defense is shown by the capacity of virus-specific CTLs via adoptive transfer to confer protection for the particular virus on non-immune recipients.
Viruses Evading Host Defense Mechanisms
A variety of viruses resist immune attack by altering their antigens continuously. Continuous antigenic variation results in the frequent emergence of new infectious strains within the influenza virus. The loss of antioxidant tolerance against these recently developing strains contributes to frequent influenza epidemics. Antigenic variation among rhinoviruses, which is the common cold causative agent, is responsible for our inability to produce an effective cold vaccine. Antigenic variation is nowhere greater than in the human immunodeficiency virus ( HIV), the AIDS causative agent. It has been estimated that HIV accumulates mutations 65 times faster than the influenza virus did.
A large number of viruses overcome the immune response by inducing widespread immunosuppression. Among these are the mumps-causing paramyxoviruses, the measles virus, Epstein-Barr virus (EBV), cytomegalovirus, and HIV. In some cases, a direct viral infection of lymphocytes or macrophages causes immunosuppression. The virus will then either directly kill, or change, the immune cells by cytolytic mechanisms. In other cases, a cytokine deficiency results in immunosuppression. For eg, EBV produces a protein, called BCRF1, homologous to IL-10; like IL-10, BCRF1 suppresses the production of cytokine by the TH1 subset, resulting in lower levels of IL-2, TNF, and IFN-γ.
Change in Viral Surface Antigens
Its variability is a distinctive feature of the influenza virus. The virus will so thoroughly change its surface antigens that the immune reaction to a virus infection that caused a prior epidemic provides little to no defense against the virus that causes a subsequent epidemic. The antigenic variation results primarily from changes protruding from the viral envelope in the spikes of hemagglutinin and neuraminidase. Antigenic variation in HA and NA is caused by two separate mechanisms: antigenic drift and antigenic shift. Antigenic drift involves a series of slowly occurring random point mutations which lead to minor changes in HA and NA. Antigenic shift results in a rapid appearance of a new influenza subtype whose HA and probably even NA differ considerably from the virus found in a previous outbreak.
Reference:
Kuby Immunology 5th Edition