We present a case of a 54 year old Guinean man, chronically infected with human immunodeficiency virus type 1 (HIV-1) subtype B, human immunodeficiency virus type 2 (HIV-2) group A and hepatitis B virus (HBV) with negative HBeAg. Previous medical conditions included hypertensive cardiac insufficiency and a chronic kidney disease.
The diagnosis of HIV-1 and HIV-2 coinfection was initially made with serological testing, initially a 4th generation assay, followed by positive HIV-1 and HIV-2 Western Blot. HIV-1 viral load was detected using a commercial assay and HIV-2 viral load was detected using an in-house real-time RT-PCR. HIV-2 resistance testing was done with an in house assay. The viral RNA was extracted from plasma using BioMerieux’s Nuclisense® EasyMag® equipment. The integrase and pol genes were amplified using a protocol in house, followed by sequencing by the Sanger method using 8 primers and the BigDye® Terminator v.3.1 Cycle Sequencing Kit. Detection and reading of DNA sequences was performed on the sequencer Automatic ABI Prism ®3100 from Applied Biosystems. Finally the DNA sequences were stored in the RegaDb database, Leuven (Rega Institute; REGA), analyzed using the CromasPro V software. 1.7.6. and interpreted according to the Grade HIV-2 algorithm (https://bit.ly/378Q3tK).
The patient was diagnosed in 2001 with an initial CD4 245 cells/uL, during pre-surgical screening. According to Centers for Disease Control and Prevention, Atlanta classification, he had category A2 disease. He had not been tested for HIV previously and was probably infected through heterosexual contact. The patient has been followed up twice a year, with viral load monitoring every 6 months in the infectious diseases’ ambulatory clinic since July 2001.
In 2001 he started ART with atazanavir/lamivudine + nelfinavir (ATV/3TC + nelfinavir). Therapy was switched to ATV/3TC + lopinavir and ritonavir (LPVr) in 2007 due to HIV-2 virologic failure [viral load (VL) = 388 cp/mL] with undetectable HIV-1 VL.
In 2011 he had another HIV-2 therapeutic failure (VL = 2771 cp/mL), with undetectable HIV-1 VL, high-grade resistance to all nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) except tenofovir disoproxil fumarate (TDF) [Q151M, M184V] and high-grade resistance to all protease inhibitors (PIs) inhibitors except for darunavir (DRV) [V47A, L90M] was shown on further testing. Therefore, ART was switched to TDF/emtricitabine + DRV/r + raltegravir.
In August 2018 he had undetectable VL to both HIV-1 and HIV-2. However, half a year later he had another virologic failure, this time to both viruses, HIV-1 (VL = 7352 cp/mL) and HIV-2 (VL = 754 cp/mL). We performed both resistance tests and HIV-2 resistance test revealed high grade resistance to all NRTIs [K65R, D67N, Q151M, S215ST] and high-grade resistance to LPV, saquinavir and DRV [V47A, I84V, L90M]. HIV-2 and HIV-1 resistance tests to integrase strand-transfer inhibitors were negative, as well as HIV-1 to PIs and reverse-transcriptase inhibitors.
Since January 2019, he has been taking tenofovir alafenamide fumarate + DTG + maraviroc and at the last evaluation he had undetectable HIV-1 and HIV-2 VL with a CD4 + cells count of 374 cells/uL. (Fig. 1).
It’s relevant to highlight that this is a patient with poor adherence to ART, who stopped ART and follow-up several times in the last years.
HBV VL has remained undetectable through all these years, without HBsAg seroconversion.
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