On Jan 21, 2011, a 57-year-old man living in France attended our emergency unit with fever, rash, lymphadenopathy, and genital ulceration, 8 days after returning from Togo. He reported sexual contact with a Togolese partner, and HIV primary infection was suspected. Fourth-generation ELISA (ARCHITECT HIV Ag/Ab Combo, Abbott, Chicago, IL) was weakly positive, and HIV-1 western blot (New Lav Blot I, Biorad, Paris, France) showed weak reactivity with the p55 and p24 antigens. On Feb 1, 2011, his HIV-1 RNA load was 4∙ 2 log10 copies per mL (Cobas TaqMan HIV-1 v2. 0 assay, Roche Molecular Systems, Branchburg, NJ, USA). On Feb 9, 2011, he developed facial paralysis. At this time his CD4 cell count was 219 per μL and his plasma and CSF HIV-1 RNA concentrations were 4∙ 4 log10 and 4∙ 5 log10 copies per mL, respectively.

In keeping with French guidelines on new cases of HIV infection, we undertook resistance genotyping before starting treatment. We were surprised that we could not amplify the reverse transcriptase and protease genes with the ViroSeq HIV-1 genotyping assay (Abbott, Chicago, IL, USA) and the French National Agency for AIDS Research consensus primers, despite the high viral load. This finding prompted us to serotype the samples. 1, 2 Clear reactivity against group-N-specific antigens was obtained and we therefore did full-length genome sequencing. 3 Phylogenetic analysis confirmed that the new sequence clustered strictly within available group-N sequences (sequence designated N1. FR. 2011, GenBank accession number JN572926). When last seen for followup after 4 weeks of antiretroviral combination therapy with tenofovir, emtricitabine, darunavir/ritonavir, raltegravir, and maraviroc, our patient’s plasma HIV-1 RNA load was below 20 copies per mL and his CD4 cell count was 483 per μL.