Dear Seran,

Please read the following text. The direct answer to your question is the example marked with bold line.

First, remember the structure and function of a virus. Once attached to its specific target cell, it injects its DNA (or RNA) into the host cell. Once inside the 'infected' cell, this viral DNA (or RNA) replicates itself as well as using the existing machinery within the 'infected' cell to make more viral proteins. It then assembles itself and can now leave this cell to infect other cells. Second, remember the structure and workings of DNA (or RNA). All the DNA strand consists of are 5-carbon deoxyribose (or ribose) sugars linked together by phosphate groups. Additionally, each 5-carbon sugar has one of four possible bases attached: A, G, C, or T. So in order to elongate a strand of DNA (or RNA), the cell simply links the 'sugar-base-phosphate' unit onto the existing 'sugar-base-phosphate' units already linked together forming the strand of DNA. We oversimplify this by saying that the DNA strand grows by adding additional bases. For example, our simplified explanation says that the DNA strand grows by adding an "A", or "G", or "C", or "T" base, one at a time. Remember that this "A", or "G" or "C" or "T" is the 'sugar-base-phosphate' unit with the base being either A, G, C, or T. Thirdly, this is an oversimplified but essentially accurate explanation of how several antiviral drugs work. The antiviral drug will be incorporated into the growing DNA (or RNA) strand as if it were another 'sugar-base-phosphate' unit. Once this drug is incorporated into the growing DNA strand, no other 'sugar-base-phosphate' units can be attached, and so any further grows stops. Hence, terminating the growth of viral DNA within the infected cell.

As an example, let's discuss acyclovir as an antiviral drug for herpes simplex infection. Acyclovir is an analog of 2-deoxyguanosine ("G"). The acyclovir is in fact modified by enzymes made only by the virus so that the acyclovir can now be incorporated into the growing viral DNA strand instead of the "G". Once incorporated, any further elongation stops because unlike "G" that should be there, the acyclovir cannot attach any further nucleoties (acyclovir cannot attach any further "A"'s, or "G"'s, or "C"'s, or "T"'s). A herpes simplex virus attaches to a susceptible host cell (seen on the right), fusing its envelope with the cell membrane, and releasing naked capsids that deliver viral DNA into the nucleus of the host cell, where it initiates the synthesis of viral DNA. Acyclovir molecules entering the cell are converted to acyclovir monophosphate by virus induced thymidine kinase enzyme. Host-cell enzymes add two more phosphates to form acyclovir triphosphate, which is transported to the nucleus. Shown in red is the cleavage of phosphate from the acyclovir triphosphate by the herpes simplex's own enzymes, the herpes simplex's DNA polymerase enzyme incorporates the acyclovir monophosphate into the growing DNA strand as if it were 2-deoxyguanosine monophosphate (a "G" base). Further elongation of the chain is impossible because acyclovir monophosphate lacks the attachment point necessary for the insertion of any additional nucleotides.

I. The acyclovir (as do other antiviral drugs) is mistakenly incorportated into the growing DNA strand. The enzymes adding in "A"'s, or "G"'s, or "C"'s, or "T"'s recognize acyclovir as a "G" and add it in.

II. The acyclovir does not have the proper structure to add any additional "A"'s, or "G"'s, or "C"'s, or "T"'s to it, and so the DNA strand cannot continue to elongate or grow. Once the acyclovir is incorporated, any further growth of viral DNA is terminated.

III. If I swallow my acyclovir drugs, isn't acyclovir going into all of my cells, and blocking the growth (or replication) of all my cell's DNA, not just the cells infected with virus? Not necessarily. As you read, the conversion of the original acyclovir into the form that is incorporated into the DNA is carried out by the virus's own enzyme. Therefore, only those cells that are infected with the virus will have this specific enzyme and convert the original acyclovir into the acyclovir that can be incorporated as a "G" base. Also, only the cells infected with virus have the enzyme that mistakenly recognizes acyclovir as a "G" base and puts it into the growing DNA strand. So, again, all of your non-virally infected cells will not that this viral enzyme and so not put acyclovir into growing DNA.

For more information, please use the following links:

http://homepage.smc.edu/wissmann_paul/anatomy1/1antiviraldrugs.html

https://en.wikipedia.org/wiki/Antiviral_drug

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3184032/

https://www.boundless.com/microbiology/textbooks/boundless-microbiology-textbook/antimicrobial-drugs-13/antiviral-drugs-159/antiviral-agents-that-prevent-virus-uncoating-or-release-799-5717/

http://www.encyclopedia.com/topic/antiviral_drug.aspx

Hoping this will be helpful,

Rafik

Dear Seran,

Please read the following text. The direct answer to your question is the example marked with bold line.

First, remember the structure and function of a virus. Once attached to its specific target cell, it injects its DNA (or RNA) into the host cell. Once inside the 'infected' cell, this viral DNA (or RNA) replicates itself as well as using the existing machinery within the 'infected' cell to make more viral proteins. It then assembles itself and can now leave this cell to infect other cells. Second, remember the structure and workings of DNA (or RNA). All the DNA strand consists of are 5-carbon deoxyribose (or ribose) sugars linked together by phosphate groups. Additionally, each 5-carbon sugar has one of four possible bases attached: A, G, C, or T. So in order to elongate a strand of DNA (or RNA), the cell simply links the 'sugar-base-phosphate' unit onto the existing 'sugar-base-phosphate' units already linked together forming the strand of DNA. We oversimplify this by saying that the DNA strand grows by adding additional bases. For example, our simplified explanation says that the DNA strand grows by adding an "A", or "G", or "C", or "T" base, one at a time. Remember that this "A", or "G" or "C" or "T" is the 'sugar-base-phosphate' unit with the base being either A, G, C, or T. Thirdly, this is an oversimplified but essentially accurate explanation of how several antiviral drugs work. The antiviral drug will be incorporated into the growing DNA (or RNA) strand as if it were another 'sugar-base-phosphate' unit. Once this drug is incorporated into the growing DNA strand, no other 'sugar-base-phosphate' units can be attached, and so any further grows stops. Hence, terminating the growth of viral DNA within the infected cell.

As an example, let's discuss acyclovir as an antiviral drug for herpes simplex infection. Acyclovir is an analog of 2-deoxyguanosine ("G"). The acyclovir is in fact modified by enzymes made only by the virus so that the acyclovir can now be incorporated into the growing viral DNA strand instead of the "G". Once incorporated, any further elongation stops because unlike "G" that should be there, the acyclovir cannot attach any further nucleoties (acyclovir cannot attach any further "A"'s, or "G"'s, or "C"'s, or "T"'s). A herpes simplex virus attaches to a susceptible host cell (seen on the right), fusing its envelope with the cell membrane, and releasing naked capsids that deliver viral DNA into the nucleus of the host cell, where it initiates the synthesis of viral DNA. Acyclovir molecules entering the cell are converted to acyclovir monophosphate by virus induced thymidine kinase enzyme. Host-cell enzymes add two more phosphates to form acyclovir triphosphate, which is transported to the nucleus. Shown in red is the cleavage of phosphate from the acyclovir triphosphate by the herpes simplex's own enzymes, the herpes simplex's DNA polymerase enzyme incorporates the acyclovir monophosphate into the growing DNA strand as if it were 2-deoxyguanosine monophosphate (a "G" base). Further elongation of the chain is impossible because acyclovir monophosphate lacks the attachment point necessary for the insertion of any additional nucleotides.

I. The acyclovir (as do other antiviral drugs) is mistakenly incorportated into the growing DNA strand. The enzymes adding in "A"'s, or "G"'s, or "C"'s, or "T"'s recognize acyclovir as a "G" and add it in.

II. The acyclovir does not have the proper structure to add any additional "A"'s, or "G"'s, or "C"'s, or "T"'s to it, and so the DNA strand cannot continue to elongate or grow. Once the acyclovir is incorporated, any further growth of viral DNA is terminated.

III. If I swallow my acyclovir drugs, isn't acyclovir going into all of my cells, and blocking the growth (or replication) of all my cell's DNA, not just the cells infected with virus? Not necessarily. As you read, the conversion of the original acyclovir into the form that is incorporated into the DNA is carried out by the virus's own enzyme. Therefore, only those cells that are infected with the virus will have this specific enzyme and convert the original acyclovir into the acyclovir that can be incorporated as a "G" base. Also, only the cells infected with virus have the enzyme that mistakenly recognizes acyclovir as a "G" base and puts it into the growing DNA strand. So, again, all of your non-virally infected cells will not that this viral enzyme and so not put acyclovir into growing DNA.

For more information, please use the following links:

http://homepage.smc.edu/wissmann_paul/anatomy1/1antiviraldrugs.html

https://en.wikipedia.org/wiki/Antiviral_drug

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3184032/

https://www.boundless.com/microbiology/textbooks/boundless-microbiology-textbook/antimicrobial-drugs-13/antiviral-drugs-159/antiviral-agents-that-prevent-virus-uncoating-or-release-799-5717/

http://www.encyclopedia.com/topic/antiviral_drug.aspx

Hoping this will be helpful,

Rafik

Well said and explaind Rafik.

For the question it is a primative mecanism of action that cand be found in almost all pharmacology books e.g Goodman and Gillman

Thank you very much Rafik, for your assistance. It is very much appreciated.

Chemotherapy of Viral Infections

Erik De Clercq.

General Concepts

Basic Mechanisms

Antiviral drugs specifically inhibit one or more steps of virus replication without causing unacceptable side effects.

Approved Antiviral Drugs

The approved antiviral drugs and the viruses and diseases they treat are amantadine and rimantadine (influenza A virus), ribavirin (respiratory syncytial virus), idoxuridine and trifluridine (topical treatment of herpetic keratitis), vidarabine and acyclovir (systemic treatment of herpes simplex virus and varicella-zoster virus infections), famciclovir and valaciclovir (oral treatment of varicella-zoster virus infections), ganciclovir and foscarnet (cytomegalovirus), and zidovudine, didanosine, zalcitabine and stavudine (human immunodeficiency virus).

Future Antiviral Drugs

To overcome the limitations of current antiviral drugs, more effective compounds are being developed that allow greater inhibition of viruses, greater selectivity for virus-specific functions, and fewer side effects, and may avoid emergence of resistant mutants.

Main Targets for Antiviral Drugs

Specific events in virus replication identified as targets for antiviral agents are viral adsorption, penetration, uncoating, and viral nucleic acid synthesis as well as viral protein synthesis. Specificity for infected cells may occur when virus-specified enzymes (e.g., thymidine kinase-induced by herpes simplex virus or varicella-zoster virus) activate drugs (e.g., acyclovir).

For more plz read at following link.

Best wishes

http://www.ncbi.nlm.nih.gov/books/NBK8119/