CD8 encephalitis in an HIVinfected patient undergoing regular antiretroviral therapy: a case report

CD8 + encephalitis, and a destructive complication of HIV, that produces severe brain damage, described in patients regularly using antiretroviral therapy. It arises by viral propagation in mononuclear phagocytes leads to persistent activation of CD8 + lymphocytes. It produces demyelinating lesions, brain infiltration by CD8 + lymphocytes, and vessel hyalinization. Magnetic resonance imaging is characterized by a large area of demyelination with a mass effect and enhancement of the ring in the image. In spite of being a potentially fatal picture, it has treatment. Case report: female patient, 43 years old, with decreased strength in MSD. HIV + for 14 years on regular use of ART (Atazanavir, Tenofovir + Lamivudine and Ritonavir), CD4 +> 400 and undetectable viral load for 3 years, Alcoholist (1-2 cans beer / day). It evolved rapidly with weakness of the right hemibody, tonic-clonic seizure, inattention, and decreased level of consciousness. Liquor- cells 21 (lymphomonocyte), analysis for viruses, bacteria, mycobacteria, and negative fungus. SARS-CoV-2 detection, Blood cultures: HTLV-I and II Antibodies screening, Serology for B and C viruses - negative. WBC: 11,600 lymphocytes 27.9%. Treated with pulse therapy with 1g for 5 days. He evolved with an improvement in the level of attention, managing to walk again without help, and remission of seizures. Discharged from hospital with oral prednisone Conclusions: CD8 + encephalitis is associated with HIV despite satisfactory control rates. With an exacerbated brain immune response, there is bilateral hypersignal in the FLAIR, punctiform or linear foci of perivascular enhancements are very suggestive. At the beginning it can manifest itself as acute or subacute neurological decline, the response to corticosteroids is dramatic.