Abstract: This invention relates to methods for determining hypersusceptibility of HIV-1 viruses to non-nucleoside reverse transcriptase inhibitors (NNRTIs) based on the viral genotypes. The methods generally comprise detecting, in a gene encoding reverse transcriptase of the HIV-1, the presence of a mutation at codon 65, 69, or 74 alone or in combination with one or more mutations at certain other codons. Combinations of mutations associated with hypersusceptibility to NNRTIs are also disclosed.

Abstract: The present invention provides a method for identifying whether a compound inhibits entry of a virus into a cell which comprises: (a) obtaining nucleic acid encoding a viral envelope protein from a patient infected by the virus; (b) co-transfecting into a first cell (i) the nucleic acid of step (a), and (ii) a viral expression vector which lacks a nucleic acid encoding an envelope protein, and which comprises an indicator nucleic acid which produces a detectable signal, such that the first cell produces viral particles comprising the envelope protein encoded by the nucleic acid obtained from the patient; (c) contacting the viral particles produced in step (b) with a second cell in the presence of the compound, wherein the second cell expresses a cell surface receptor to which the virus binds; (d) measuring the amount of signal produced by the second cell in order to determine the infectivity of the viral particles; and (e) comparing the amount of signal measured in step (d) with the amount of signal produced

Abstract: Provided are methods for identifying whether a compound inhibits entry of a virus into a cell. The method may include obtaining nucleic acid encoding a viral envelope protein from a patient infected by the virus and co-transfecting it into a first cell along with a viral expression vector which lacks a nucleic acid encoding the envelope protein. The method may further include contacting the viral particles produced by the first cell with a second cell to which the virus binds in the absence and presence of the compound and measuring the amount of signal produced by the second cell.

Abstract: Provided are methods for identifying whether a compound inhibits entry of a virus into a cell. The method may include obtaining nucleic acid encoding a viral envelope protein from a patient infected by the virus and co-transfecting it into a first cell along with a viral expression vector which lacks a nucleic acid encoding the envelope protein. The method may further include contacting the viral particles produced by the first cell with a second cell to which the virus binds in the absence and presence of the compound and measuring the amount of signal produced by the second cell.

Abstract: The present invention provides a method for identifying whether a compound inhibits entry of a virus into a cell which comprises: (a) obtaining nucleic acid encoding a viral envelope protein from a patient infected by the virus; (b) co-transfecting into a first cell (i) the nucleic acid of step (a), and (ii) a viral expression vector which lacks a nucleic acid encoding an envelope protein, and which comprises an indicator nucleic acid which produces a detectable signal, such that the first cell produces viral particles comprising the envelope protein encoded by the nucleic acid obtained from the patient; (c) contacting the viral particles produced in step (b) with a second cell in the presence of the compound, wherein the second cell expresses a cell surface receptor to which the virus binds; (d) measuring the amount of signal produced by the second cell in order to determine the infectivity of the viral particles; and (e) comparing the amount of signal measured in step (d) with the amount of signal produced

Abstract: This invention relates, in part, to methods and compositions for determining altered susceptibility of a human immunodeficiency virus (“HIV”) to the non-nucleoside reverse transcriptase inhibitors (“NNRTIs”) efavirenz (“EFV”), nevirapine (“NVP”), and delavirdine (“DLV”), the nucleoside reverse transcriptase inhibitor AZT, and the integrase strand transfer inhibitors diketo acid 1, diketo acid 2, and L-870,810 by detecting the presence of a mutation or combinations of mutations in the gene encoding HIV reverse transcriptase that are associated with altered susceptibility to the anti-HIV drugs.

Abstract: This invention relates to methods for determining hypersusceptibility of HIV-1 viruses to non-nucleoside reverse transcriptase inhibitors (NNRTIs) based on the viral genotypes. The methods generally comprise detecting, in a gene encoding reverse transcriptase of the HIV-1, the presence of a mutation at codon 65, 69, or 74 alone or in combination with one or more mutations at certain other codons. Combinations of mutations associated with hypersusceptibility to NNRTIs are also disclosed.

Abstract: This invention relates, in part, to methods and compositions for determining altered susceptibility of a human immunodeficiency virus (“HIV”) to the non-nucleoside reverse transcriptase inhibitors (“NNRTIs”) efavirenz (“EFV”), nevirapine (“NVP”), and delavirdine (“DLV”), the nucleoside reverse transcriptase inhibitor AZT, and the integrase strand transfer inhibitors diketo acid 1, diketo acid 2, and L-870,810 by detecting the presence of a mutation or combinations of mutations in the gene encoding HIV reverse transcriptase that are associated with altered susceptibility to the anti-HIV drugs.

Abstract: This invention relates to methods for determining hypersusceptibility of HIV-1 viruses to non-nucleoside reverse transcriptase inhibitors (NNRTIs) based on the viral genotypes. The methods generally comprise detecting, in a gene encoding reverse transcriptase of the HIV-1, the presence of a mutation at codon 65, 69, or 74 alone or in combination with one or more mutations at certain other codons. Combinations of mutation associated with hypersusceptibility to NNRTIs are also disclosed.

Abstract: This invention relates, in part, to methods and compositions for determining altered susceptibility of a human immunodeficiency virus (“HIV”) to the non-nucleoside reverse transcriptase inhibitors (“NNRTIs”) efavirenz (“EFV”), nevirapine (“NVP”), and delavirdine (“DLV”), the nucleoside reverse transcriptase inhibitor AZT, and the integrase strand transfer inhibitors diketo acid 1, diketo acid 2, and L-870,810 by detecting the presence of a mutation or combinations of mutations in the gene encoding HIV reverse transcriptase that are associated with altered susceptibility to the anti-HIV drugs.

Abstract: This invention relates to antiviral drug susceptibility and resistance tests to be used in identifying effective drug regimens for the treatment of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS), particularly treatment regimens including a protease inhibitor. The invention further relates to the means and methods of monitoring the clinical progression of HIV infection and its response to antiretroviral therapy using phenotypic or genotypic susceptibility assays.

Abstract: The present invention provides an approach for developing an algorithm for determining the effectiveness of anti-viral drugs based on a comprehensive analysis of paired phenotypic and genotypic data guided by phenotypic clinical cut-offs. In one aspect, the algorithm allows one to provide a patient with effective treatment. It helps predict whether an infected individual will respond to treatment with an anti-viral compound, thereby allowing an effective treatment regimen to be designed without subjecting the patient to unnecessary side effects. Also, by avoiding the administration of ineffective drugs, considerable time and money is saved.

Abstract: The present invention provides a method for identifying whether a compound inhibits entry of a virus into a cell which comprises: (a) obtaining nucleic acid encoding a viral envelope protein from a patient infected by the virus; (b) co-transfecting into a first cell (i) the nucleic acid of step (a), and (ii) a viral expression vector which lacks a nucleic acid encoding an envelope protein, and which comprises an indicator nucleic acid which produces a detectable signal, such that the first cell produces viral particles comprising the envelope protein encoded by the nucleic acid obtained from the patient; (c) contacting the viral particles produced in step (b) with a second cell in the presence of the compound, wherein the second cell expresses a cell surface receptor to which the virus binds; (d) measuring the amount of signal produced by the second cell in order to determine the infectivity of the viral particles; and (e) comparing the amount of signal measured in step (d) with the amount of signal produced

Abstract: This invention relates to methods for determining altered susceptibility of HIV-I viruses to protease inhibitors (PIs) based on the viral genotypes. The methods generally comprise detecting, in a gene encoding protease and/or gag of the HIV-I, the presence of mutations correlated with altered susceptibility to amprenavir and/or darunavir.

Abstract: The present invention provides methods and devices for predicting whether an HIV-I is likely to have a reduced susceptibility to an antiviral drug based on the HIV-I's genotype. In one aspect, the invention provides methods comprising determining whether a mutation or combination of mutations associated with altered susceptibility to protease inhibitors are present, as disclosed herein, thereby assessing the effectiveness of tipranavir therapy in the HIV-infected subject. Computer implemented methods comprising determining HIV-I's altered susceptibility are provided.

Abstract: This invention relates to methods for determining hypersusceptibility of HIV-1 viruses to non-nucleoside reverse transcriptase inhibitors (NNRTIs) based on the viral genotypes. The methods generally comprise detecting, in a gene encoding reverse transcriptase of the HIV-1, the presence of a mutation at codon 65, 69, or 74 alone or in combination with one or more mutations at certain other codons. Combinations of mutation associated with hypersusceptibility to NNRTIs are also disclosed.

Abstract: The present invention provides an approach for developing an algorithm for determining the effectiveness of anti-viral drugs based on a comprehensive analysis of paired phenotypic and genotypic data guided by phenotypic clinical cut-offs. In one aspect, the algorithm allows one to provide a patient with effective treatment. It helps predict whether an infected individual will respond to treatment with an anti-viral compound, thereby allowing an effective treatment regimen to be designed without subjecting the patient to unnecessary side effects. Also, by avoiding the administration of ineffective drugs, considerable time and money is saved.

Abstract: This invention relates, in part, to methods and compositions for determining altered susceptibility of a human immunodeficiency virus (“HIV”) to the non-nucleoside reverse transcriptase inhibitors (“NNRTIs”) efavirenz (“EFV”), nevirapine (“NVP”), and delavirdine (“DLV”), the nucleoside reverse transcriptase inhibitor AZT, and the integrase strand transfer inhibitors diketo acid 1, diketo acid 2, and L-870,810 by detecting the presence of a mutation or combinations of mutations in the gene encoding HIV reverse transcriptase that are associated with altered susceptibility to the anti-HIV drugs.

Abstract: This invention relates to methods for determining resistance of HIV-I viruses to protease inhibitors (PIs) based on the viral genotypes. The methods generally comprise detecting, in a gene encoding protease of the HIV-I, the presence of a mutation in at least one of codon 22, 69, 74, or 83 alone or in combination with one or more mutations at certain other codons, or, in a gene encoding gag of the HIV-I, the present of a mutation in at least one of codon 418 or 482 alone or in combination with one or more mutations at certain other codons. Combinations of mutations associated with resistance to PIs are also disclosed.

Abstract: The present invention provides methods and devices for predicting whether an HIV-1 is resistant to an antiviral drug based on the HIV-1's genotype. In one aspect, the invention provides methods comprising determining whether a mutation or combination of mutations associated with NRTI resistance are present, as disclosed herein, thereby assessing the effectiveness of FTC therapy in the HIV-infected subject. Computer implemented methods comprising determining HIV-1 resistance are provided.