Antiviral agents

The most common adverse effects associated with antiretroviral regimens containing enfuvirtide are local injection site reactions with resultant pain, erythema, induration, nodules and cysts, pruritus, and ecchymosis. These reactions have been reported to occur in 98% of patients, but only a small minority needed to stop therapy. Other very common adverse effects include nausea, diarrhoea, weight loss, and peripheral neuropathy.

The most common adverse effects associated with antiretroviral regimens containing emtricitabine are headache, diarrhoea, and nausea; hyperpigmented skin discoloration is very common in children and common in adults. Other common adverse effects include abdominal pain, vomiting, dyspepsia, abnormal dreams, asthenia, dizziness, insomnia, pain, allergic skin reactions, pruritus, rashes, and urticaria. Abnormal laboratory test results associated with emtricitabine-containing regimens include hyperbilirubinaemia, increases in serum lipase and pancreatic amylase, and raised liver enzymes. There have also been reports of neutropenia and anaemia.

Didanosine is converted intracellularly to its active form dideoxyadenosine triphosphate. This triphosphate halts the DNA synthesis of retrovirases, including HIV, through competitive inhibition of reverse transcriptase and incorporation into viral DNA.

Delavirdine acts by non-competitive inhibition of HIV-1 reverse transcriptase; it binds to the enzyme, disrupting the conformation of its catalytic site and impairing its RNA- and DNA-dependent polymerase activity. Resistance to delavirdine and emergence of cross-resistance to other non-nucleoside reverse transcriptase inhibitors has been seen.

Darunavir is a selective inhibitor of HIV-1 protease. It interferes with the formation of essential viral proteins making them incapable of infecting other cells. Viral resistance develops rapidly when HIV-protease inhibitors are given alone and therefore they are used with other antiretrovirals.

Cidofovir undergoes intracellular phosphorylation by cellular kinases to the antiviral metabolite, cidofovir diphosphate, which acts as a competitive inhibitor of viral DNA polymerase. It is active against a range of herpesviruses including CMV, and, since its activity is not reliant on viral enzymes, may retain activity against some aciclovir- and foscarnet-resistant viruses. Cross-resistance with ganciclovir is common.

Atazanavir is a selective, competitive, reversible inhibitor of HIV-1 protease. It interferes with the formation of essential viral proteins making them incapable of infecting other cells. Viral resistance develops rapidly when HIV-protease inhibitors are given alone and therefore they are used with other antiretrovirals.

Amprenavir is an HIV-protease inhibitor with antiviral activity against HIV. ft is used in the treatment of HIV infection and AIDS. Viral resistance emerges rapidly when amprenavir is used alone, and it is therefore used with other antiretrovirals.

Adefovir is converted intracellularly in stages to the di-phosphate, which then inhibits the DNA synthesis of hepatitis B virus through competitive inhibition of reverse transcriptase and incorporation into viral DNA. At high doses it has some activity against HIV.

Abacavir is converted intracellularly in stages to its active form carbovir triphosphate. This halts the DNA synthesis of retroviruses, including HIV, through competitive inhibition of reverse transcriptase and incorporation into viral DNA.