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THE PHARMA REVIEW (MAY - JUNE 2011)

Acquired Immune Deficiency Syndrome

Dr Ravinder N. Kaul

Summary
Of all the viruses that have plagued human beings through the ages, few have cast darker shadows or proved more formidable than one that causes acquired immune deficiency syndrome AIDS. Unless treated, infection leads to premature death in all or almost all of those affected. The need for effective treatment to prevent and to arrest the degenerative progress of the disease is both urgent and obvious. Drugs have been AIDS patients’ greatest objects and hope. Many of them like azidothymidine AZT are aimed at blocking reverse transcriptase, the enzyme that enables the AIDS virus to convert its RNA into DNA within the cell and begin reproducing. This article presents the biology of AID virus and the mechanism of nucleoside analogues directed to treat the infection.
Introductions
The word virus comes from Latin for slimy liquid, stench, poison and connotation is appropriate, not only for the AIDS virus but for the untold number of varieties that have been preying on the animals and plants since long before Homo sapiens appeared on earth. Indeed the current AIDS and swine flu epidemics are a grim reminder that these infinitesimal, bizarre creatures may be mankind’s deadliest enemy. Viruses, unlike bacteria, are totally dependent upon the cell they infest for much of the metabolic machinery required for their replication. Therefore, for an antiviral agent to be effective, it must be able to selectively inhibit virus replication without disrupting normal cellular functions. This selectively must be based on exploitable biochemical differences that exist between the processes involved in virus replication and those involved in replication of a normal cell. A number of virus specific sites which are amenable to antiviral intervention have been identified (e.g., adsorption, penetration, uncoating, synthesis of viral nucleic acids, synthesis of viral proteins, assembly, maturation and release). Of particular interest are the findings that the replication of many viruses involves enzymes specifically coded for by the virus (e.g., RNA polymerase, DNA polymerase, reverse transcriptase, nucleases, kinases, ribonucleotide reductase, methylases, guanyltransferase and proteases). These viral enzymes display characteristics that are quite distinct from their host cell counterparts and, therefore, are important targets for the design of selective antiviral agents.

 

 

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The above content is an abstract only. For the full Article please contact:
KONGPOSH Publications Pvt. Ltd.
ICS House, C-19, Commercial Complex, SDA, Opp. IIT Gate, New Delhi, India -110016
Tel.: 26855839, 9811195411
Email: kongposhpub@gmail.com, Website: http://www.kppub.com

 
 
 
 

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