Evaluation of Lymph Node Virus Burden in Human Immunodeficiency Virus–Infected Patients Receiving Efavirenz‐Based Protease Inhibitor–Sparing Highly Active Antiretroviral Therapy
Author(s) -
Mark Dybul,
TaeWook Chun,
Douglas Ward,
Kurt Hertogs,
Brendan Larder,
Cecil H. Fox,
Jan M. Orenstein,
Barbara Baird,
Yuexia Li,
Linda G. Green,
Delphine Engel,
Shuying Liu,
JoAnn M. Mican,
Anthony S. Fauci
Publication year - 2000
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/315407
Subject(s) - efavirenz , virology , viremia , virus , biology , lymph node , viral load , viral replication , reverse transcriptase inhibitor , lentivirus , protease inhibitor (pharmacology) , immunology , viral disease , antiretroviral therapy
Although efavirenz-containing regimens effectively suppress plasma levels of human immunodeficiency virus (HIV) RNA, it is now clear that undetectable plasma viremia may not reflect a lack of viral replication. Because lymphoid tissue is an active site of HIV replication, the lymph node virus burden was analyzed in persons who received highly active antiretroviral therapy (HAART) containing either efavirenz or a protease inhibitor (PI). Testing with in situ hybridization revealed no detectable follicular dendritic cell-associated HIV RNA in either group, and only 2 of 8 persons in the efavirenz group and 1 of 4 in the PI group had detectable RNA in lymph node mononuclear cells (LNMC) when tested by use of nucleic acid sequencebased amplification. Low levels of replication-competent HIV were identified in both groups by use of quantitative coculture assays. There was no evidence of development of resistance to either regimen in virus isolated from LNMC. These data support the use of efavirenz as an alternative to a PI in initial HAART regimens.
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