A 55-year-old man coinfected by HIV-1 subtype B and hepatitis C virus (HCV) genotype 3a since 1984 through intravenous drug use (IVDU). The patient was an HIV elite controller, displaying… Click to show full abstract
A 55-year-old man coinfected by HIV-1 subtype B and hepatitis C virus (HCV) genotype 3a since 1984 through intravenous drug use (IVDU). The patient was an HIV elite controller, displaying undetectable HIV plasma viral load (HIV-pVL) since HIV infection diagnosis, with CD4þ and CD8þ T-cell counts more than 1000 cells/ml and CD4þ : CD8þ ratio less than 1 (Fig. 1a and b), Centers for Disease Control and Prevention (CDC) classification system stage B3, never exposed to antiretroviral therapy. The patient was a heavy smoker (60 pack-year) and had rehabilitated from alcohol abuse in 2010. In May 2012, he was diagnosed with lung adenocarcinoma of the upper right lobe with mediastinal infiltration (cT3N2-bulkyM0, grade IIIb) on chestcomputed tomography (CT) for investigation of a persistent cough. From June 2012 to November 2012, he received four cycles of radio-chemotherapy with cisplatine/pemetrexed and prophylaxis against opportunistic infections. CD4þ cell counts dropped by 25% at diagnosis and by 75% after radio-chemotherapy (Fig. 1b). HIV-pVL blipped to 75 copies/ml but suppressed spontaneously after 1 month. High proportions of activated CD8þHLA-DRþ (Fig. 1c; 66.3%, normal range <10%) and CD8þCD38þ cells (44.3%, normal range 5–17%), and of CD8þCD28 senescent cells (49.9%, normal range 20–30% [1]) were found before introduction of chemotherapy. Radio-chemotherapy resulted in 26% reduction of the primary tumour. Facing relapse in July 2013, the patient received three cycles of carboxyplatin/pemetrexed, but presented with complete right lung atelectasis that persisted despite endobronchial debulking and stent, leading to death of the patient in December 2013.
               
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