The New Nation - Internet Edition

Tia

A range of effects on host cells that can be caused by a virus fall into several categories.

Some viruses do not produce pathological detriment - these infections are asymptomatic.

Some viruses, e.g. picornaviruses, described as cytocidal, quickly kill their host cell - releasing. Non-cytocidal viruses replicate and release their progeny without killing the host cell immediately, e.g. influenza, or even at all, like herpes virus. Cytocidal and non-cytocidal viruses both cause acute infections in their hosts.

Sometimes a virus will infect a cell, produce few or no progeny, and the host cell remains largely intact. This type of viral infection is described as persistent e.g. the HIV virus.

Viruses usually produce harmful effects. These alterations in host cells/tissues are described as cytopathic effects-they may appear rounded up, or their nuclei may be swollen, and some cells may even fuse to form giant cells called syncytia.

An infected cells metabolism is corrupted and they can often no longer synthesize protein Pathogenic viruses, especially, cytocidal ones, produce factors that inhibit the synthesis of host DNA, RNA and protein, like the polio virus, which produces proteins known as 2A and 3C that inhibit host cell translation and transcription respectively.

It is not completely known how these viruses kill their host cell as they die before they have exhausted their protein supplies. It could be that the integrity of the plasma membrane is compromised.

Damage to the plasma membrane may lead to the death of the host cell. This is because different concentrations of Na+ions and K+ions inside and outside the cell may no longer be maintained, and dissipation of these ion gradients can have consequences

i.e. osmotic lysis. Infected cells are often found to have viral proteins in their plasma membranes. The immune system recognises them as foreign antigens, and responds accordingly. Alterations to the membranes of a group of infected cells can lead to the membranes fusing to form a giant, multinucleate cell (the syncytia seen in culture). Such cells are observed in measles and HN infections, where upto 50 or 100 cells can conglumerate.

Viruses can also damage intracellular membranes e.g. those of lysosomes, allowing the egradative anzymes to leak out, leading to self-digestion and consequent lysis.

The granules of inclusion bodies consist of sites where new viral components are being synthesized. These sites may be found in the cytosol or the nucleus, depending on the virus involved, and can detriment the cell's ultrastructure.

Poxviruses form inclusion bodies in the cytoplasm, whereas the measles virus forms them in both the cytoplasm and the nucleus. Adenoviruses are assembled in the nucleus. The newly synthesised viral components often pack together to form a crystal-like structure known as a paracrystal line array.

Viruses that penetrate the cell nucleus, e.g adenoviruses and herpes viruses, may disrupt the chromosomes.

Viral replication needs a living/functioning cell, so the host cell is not killed until the progeny have been produced. But, it is in the host's interest that the virally infected cell should die immediately.

Apoptosis-programmed cell death - is thus an important mechanism of host defence, and is demonstrated by cells infected with viruses such as HIV, influenza and picomaviruses. Viruses, though, have evolved their counterstrategies.

Many viral proteins are toxic to the host, because of high concentrations or they may have a morphological change. An example of this is the gp120 viral envelope protein of HIV, which triggers apoptosis in neurons by altering the intracellular concentration of calcium ions.

Cellular effects can cause illness in an individual infected with a virus. Numerous viruses cause acute infections leading to a rapid onset of symptoms followed by recovery, and complete elimination of the virus from the body.

Conversely, viruses can cause persistent infections, here the virus stays in the host for an extended period. They stop any cytopathic activity and successfully invade the immune system. Some viruses adapt both strategies: Varicella zoster, the herpesvirus that causes chickenpox, also causes a type of persistent infection described as latent.

Concluding the acute chickenpox infection, the virus persists in the sensory nerves without replicating and is undetectable i.e. latent. Years later, the virus can reactivate, on several occasions, to produce the skin disease shingles.

Another type of persistent infection is called a slow infection, because following an initial acute stage, the virus eventually brings about symptoms that kill the host e.g. subacute sclerosing panencephalitis, which may be caused by the measles virus.

Some infections with DNA viruses or retroviruses can detriment a cell by altering its behaviour. Transformation is sometimes affiliated with integration of viral nucleic acid into the host genome, disturbing the genetic sequence, so lacking the regulatory mechanisms and may grow quicker than its neighbours. These cells can cause cancer e.g. some types of cervical cancer have been linked with certain papilloma viruses.