Abstract
Background Even though, Highly Active Antiretroviral Therapy (HAART) has resulted in significant reduction in mortality associated with Acquired Immune Deficiency Syndrome (AIDS), the side-effects and difficulties in patient compliance warrants the search for new therapeutic options. One potential strategy is to design chemokine analogues that will prevent the entry of human immunodeficiency virus-1 (HIV-1) into the target cell by competitively blocking its interaction with CC chemokine-5 (CCR5) receptor. The objective of the present study is to design and validate the efficacy of chemokine analogues based on the viral macrophage inflammatory protein-II (vMIP-II) core as putative anti-HIV agents.
Highlights
Even though, Highly Active Antiretroviral Therapy (HAART) has resulted in significant reduction in mortality associated with Acquired Immune Deficiency Syndrome (AIDS), the side-effects and difficulties in patient compliance warrants the search for new therapeutic options
One potential strategy is to design chemokine analogues that will prevent the entry of human immunodeficiency virus-1 (HIV-1) into the target cell by competitively blocking its interaction with CC chemokine-5 (CCR5) receptor
The objective of the present study is to design and validate the efficacy of chemokine analogues based on the viral macrophage inflammatory protein-II core as putative anti-HIV agents
Summary
Active Antiretroviral Therapy (HAART) has resulted in significant reduction in mortality associated with Acquired Immune Deficiency Syndrome (AIDS), the side-effects and difficulties in patient compliance warrants the search for new therapeutic options. The objective of the present study is to design and validate the efficacy of chemokine analogues based on the viral macrophage inflammatory protein-II (vMIP-II) core as putative anti-HIV agents
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