The host immune response to viruses is both humoral and cell-mediated. Circulating antibody will 
neutralise extracellular virus in the body fluids (including mucous membranes) and the cell-mediated 
arm will attack cells that express viral proteins. Previous infection or vaccination will be the two 
relevant factors that dictate whether a person is able to swiftly neutralise an infection or not. In light of 
these protective mechanisms, viruses have developed strategies to try to minimise their contact with the 
immune response of the host. Viruses have adopted various strategies to out-manoeuvre the host, in 
particular to evade or suppress the immune response that attempts to develop antiviral products. 

It is useful to consider the broader strategies before looking at cellular mechanisms.
•  Evasion of immune response.Viruses can replicate in tissues that are relatively protected from 
surveillance by immune cells (e.g. brain, dermis). Alternatively, they can avoid extracellular stages 
in the course of infection. Fusion of infected cells, budding within cell vesicles and replication 
within lymphocytes all avoid exposure to neutralising antibodies. 
•  Suppression of immune response.Some virus infections infect the immune cells that mount the 
immune response in order to suppress them. Strategically this makes good sense; hence, many 
viruses infect lymphocytes, e.g. B lymphocytes are infected by EBV and T lymphocytes are 
infected by HIV. (It is interesting to note that intracellular bacteria tend to infect macrophages, e.g. 
Mycobacterium tuberculosis.) 
Virus infections of the neutrophils appear to be either unusual or of little value to the virus, possibly 
because neutrophils do not live long enough for adequate viral replication. Neutrophils live for only 12–
18 hours, whereas lymphocytes and macrophages have long lifespans which make them worthwhile 


As we have seen, the first line response (innate immunity) of the host to viral infections is dominated by 
the actions of the chemokines called interferons. Interferon will need to contain viral infection until the 
specific immunity has developed. Many viruses have developed the ability to block the actions of 
interferon-based responses by producing proteins that interfere at various points in the action of the 

different chemokines/cytokines. It is obvious that viruses need to thwart the early attempts of the immune system to kill them. In order to multiply and then exit the host before the specific immunity 
develops, the virus must suppress the innate immunity for as long as possible. It has been pointed out 
that total suppression of the immune response is not a feature of viral infections. Despite being costly in 
terms of genome space for the virus, this strategy will be of benefit since it wants to multiply in the host 
at the expense of other invading parasites. Selective suppression of the innate immunity still enables the 
host to repel other pathogens. 
The host response to virus infection will generate extracellular signals (cytokines) and these will bind to 
cell receptors and trigger intracellular events that will aim to inhibit viral replication. It follows that viruses can inhibit both the extracellular and intracellular signalling events. The following list illustrates how viruses have attempted to modulate various points of the immune response.
•  Minimise recognition by the host.For viruses that cause systemic infections, the first entry of 
virus into the bloodstream during a viraemic phase will attract the attention of Complement 
components. Certain viruses produce molecular mimics (homologues) of Complement components 
which will block the Complement cascade attacking the free virion. These homologues are termed 
viroceptors. Mimicry is also used by enveloped viruses which include host proteins in the viral 
envelope to mask their recognition as ‘foreign’. Virus-infected cells also secrete proteins that 
suppress their recognition by Complement, thereby protecting the manufacture of new virus. 
•  Inhibit production of interferon.Interferon production is an important early step in the defence 
against virus infections. Viruses need to interfere with the action of interferon to establish an 
infection. One way to counter the action of interferon, is for viruses to secrete molecular mimics of 
IFN receptors. In this way IFN binds to the competing mimic receptor rather than real receptor on 
the virus-infected cell. As molecular mimics of receptors, they are called viroceptors. Other viral 
proteins have been found to target the cellular signalling pathways that occur following binding of 

IFN to the cell receptor. 
Modulation of cytokine action.The mechanisms that viruses target when interfering with the 
action of cytokines, most notably interferon, may be at any point in the communication network 
employed by cytokines: 
interfering with cytokine production by cells
inhibiting cytokine binding to cells and 
interfering with the intracellular action of cytokines

The action of viruses on cytokines, however, is not always inhibitory. Some viruses actually recruit 
cytokines that promote cellular proliferation. In this way the net production of the virus will be 
•  Prevent apoptosis.Apoptosis, programmed cell suicide, occurs only if a cell receives a signal to 
proceed. That signal may be triggered by the presence of a virus. In general, viruses try to prevent 
the cell from carrying out this self-destruction and numerous examples exist of viruses producing 
proteins that inhibit apoptosis. Apoptosis of eukaryotic cells can be triggered following activation 
of proteins such as p53 and ICE-like proteases. Certain viruses produce proteins that inhibit the 
functioning of these two triggers. 
In order to produce viroceptors and other homologues, the virus must possess sufficient gene space. This 
is only possible in the larger DNA viruses such as Herpes and pox viruses. RNA viruses do not have the 
genome size to carry the necessary protein coding. To compensate, RNA viruses will more often choose 

to outwit the host by exploiting the genetic plasticity inherent in replicating RNA. One of the mechanisms for creating genetic variability and thereby generating time whilst the host develops specific 
immunity is antigenic variation. The host has spent a week manufacturing immunity against the original strain of virus but antigenic variation creates a new strain against which the host is immunologically na├»ve. 

Cited By Kamal Singh Khadka
Msc Microbiology, TU.
Assistant Professor In PU, PBPC, PNC, LA, NA.
Pokhara, Nepal.

www.ncbi.nlm.nih.gov › NCBI › Literature › Bookshelf
www.ncbi.nlm.nih.gov › Journal List › Elsevier Sponsored Documents
micro.med.harvard.edu › Faculty


Popular posts from this blog

Stains/ Dyes


Contributions Of Antony Van Leeuwenhoek & Louis Pasteur