Greg Barrett P.A.
Physician Assistant | Medical
105 MEDICAL PLZ SULPHUR SPRINGS TX, 75482About
Greg Barrett is a physician assistant practicing in SULPHUR SPRINGS, TX. Greg specializes in preventing and treating human illness and injury by providing a broad range of care under the supervision of a physician. A physician assistant's work can include physical exams, ordering and interpreting tests, performing procedures and prescribing medication. Often times, they can assist in surgery but the scope of practice can vary according to jurisdiction or health care setting.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Genotyping of acute HBV isolates from England, 1997-2001.
- Comparative biochemical analysis of HIV-1 subtype B and C integrase enzymes.
- Stage-dependent inhibition of HIV-1 replication by antiretroviral drugs in cell culture.
- Expression of Nef from unintegrated HIV-1 DNA downregulates cell surface CXCR4 and CCR5 on T-lymphocytes.
- Identification of novel mutations responsible for resistance to MK-2048, a second-generation HIV-1 integrase inhibitor.
- Neither ritonavir nor darunavir affect cell surface expression of tetherin or Vpu-mediated tetherin down-modulation.
- HIV-1 subtype B and C integrase enzymes exhibit differential patterns of resistance to integrase inhibitors in biochemical assays.
- Tetherin restricts direct cell-to-cell infection of HIV-1.
- Transcription of preintegrated HIV-1 cDNA modulates cell surface expression of major histocompatibility complex class I via Nef.
- The role of unintegrated DNA in HIV infection.
- Vpu-mediated tetherin antagonism of ongoing HIV-1 infection in CD4(+) T-cells is not directly related to the extent of tetherin cell surface downmodulation.
- The HIV-1 Vpu viroporin inhibitor BIT225 does not affect Vpu-mediated tetherin antagonism.
- The viral protein Tat can inhibit the establishment of HIV-1 latency.
- Novel therapeutic strategies targeting HIV integrase.
- Maraviroc and other HIV-1 entry inhibitors exhibit a class-specific redistribution effect that results in increased extracellular viral load.
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