<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cole AM</submitter><funding>NIAID NIH HHS</funding><pagination>1813-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC122276</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>99(4)</volume><pubmed_abstract>Human bone marrow expresses a pseudogene that encodes an antimicrobial peptide homologous to rhesus monkey circular minidefensins (delta-defensins). We prepared the putative ancestral human peptide by solid-phase synthesis and named it "retrocyclin." Retrocyclin did not cause direct inactivation of HIV-1, and its modest antibacterial properties resembled those of its rhesus homologs. Nevertheless, retrocyclin had a remarkable ability to inhibit proviral DNA formation and to protect immortalized and primary human CD4(+) lymphocytes from in vitro infection by both T-tropic and M-tropic strains of HIV-1. Confocal fluorescent microscopy studies performed with BODIPY-FL-labeled RC-101, a close analog of retrocyclin, showed that the peptide formed patch-like aggregates on the surface of CD4(+) cells. These findings suggest that retrocyclin interferes with an early stage of HIV-1 infection and that retrocyclin-like agents might be useful topical agents to prevent sexually acquired HIV-1 infections.</pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Retrocyclin: a primate peptide that protects cells from infection by T- and M-tropic strains of HIV-1.</pubmed_title><pmcid>PMC122276</pmcid><funding_grant_id>AI37945</funding_grant_id><funding_grant_id>AI43202</funding_grant_id><funding_grant_id>AI22839</funding_grant_id><funding_grant_id>P01 AI037945</funding_grant_id><funding_grant_id>R01 AI052017</funding_grant_id><pubmed_authors>Boo LM</pubmed_authors><pubmed_authors>Yang OO</pubmed_authors><pubmed_authors>Bristol G</pubmed_authors><pubmed_authors>Zack JA</pubmed_authors><pubmed_authors>Zhao C</pubmed_authors><pubmed_authors>Nguyen T</pubmed_authors><pubmed_authors>Hong T</pubmed_authors><pubmed_authors>Waring AJ</pubmed_authors><pubmed_authors>Cole AM</pubmed_authors><pubmed_authors>Lehrer RI</pubmed_authors></additional><is_claimable>false</is_claimable><name>Retrocyclin: a primate peptide that protects cells from infection by T- and M-tropic strains of HIV-1.</name><description>Human bone marrow expresses a pseudogene that encodes an antimicrobial peptide homologous to rhesus monkey circular minidefensins (delta-defensins). We prepared the putative ancestral human peptide by solid-phase synthesis and named it "retrocyclin." Retrocyclin did not cause direct inactivation of HIV-1, and its modest antibacterial properties resembled those of its rhesus homologs. Nevertheless, retrocyclin had a remarkable ability to inhibit proviral DNA formation and to protect immortalized and primary human CD4(+) lymphocytes from in vitro infection by both T-tropic and M-tropic strains of HIV-1. Confocal fluorescent microscopy studies performed with BODIPY-FL-labeled RC-101, a close analog of retrocyclin, showed that the peptide formed patch-like aggregates on the surface of CD4(+) cells. These findings suggest that retrocyclin interferes with an early stage of HIV-1 infection and that retrocyclin-like agents might be useful topical agents to prevent sexually acquired HIV-1 infections.</description><dates><release>2002-01-01T00:00:00Z</release><publication>2002 Feb</publication><modification>2025-05-31T23:23:43.936Z</modification><creation>2019-03-27T00:17:09Z</creation></dates><accession>S-EPMC122276</accession><cross_references><pubmed>11854483</pubmed><doi>10.1073/pnas.052706399</doi></cross_references></HashMap>