Background Selection of the K103N mutation is associated with a small but significant reduction in viral replicative fitness. Therefore it could be hypothesised that transmission of this strain could be associated with minimal symptoms and low level viraemia at HIV seroconversion.

Case We present the case of a 41-year-old MSM who was admitted with fever, confusion and agitation following unprotected anal sex 6 weeks earlier with a man of unknown HIV status. He required intubation due to the level of agitation. Admission CT and MRI brain were unremarkable. The first test HIV test was weakly antibody positive; a repeat 6 days later showed a stronger antibody response consistent with HIV seroconversion. His baseline CD4 count was 138 (18%); HIV viral load was 929 000 copies/ml. CSF analysis showed 4 white blood cells, elevated protein at 1.2 g/dl, and a normal CSF to plasma glucose ratio. There was insufficient CSF sample for HIV viral load testing. A diagnosis of encephalitis secondary to HIV seroconversion was made and antiretroviral therapy (ART) with five drugs was started on day 3 of admission. The patient remained agitated for several days. By day 21 the seroconversion symptoms had fully resolved, and by day 28 the plasma HIV viral load was undetectable. Viral genotyping showed the K103N mutation only. The patient remains on ART; now simplified to Kivexa, Darunavir and Ritonavir. This is to continue for 48 weeks at which point a decision will be made to either stop treatment or to continue lifelong ART.

Conclusion Transmitted drug resistant HIV can cause severe seroconversion illness and high levels of viraemia despite lower viral fitness. To our knowledge, this is the first report of viral encephalitis at HIV seroconversion caused by drug resistant HIV. The role of entry inhibitors and integrase inhibitors for the treatment of severe seroconversion symptoms to prevent viral entry into cells and aid rapid decline in viraemia are currently under evaluation.