BICtegravir Single Tablet Regimen is a multiregional, observational cohort study assessing the effectiveness and safety of bictegravir/emtricitabine/tenofovir alafenamide (B/F/TAF) in treatment-naïve (TN) and treatment-experienced (TE) people with HIV. We present 24-month data for the BICtegravir Single Tablet Regimen Asia cohort. Between December 2020 and March 2024, prospective and retrospective data were collected from TN and TE people with HIV receiving B/F/TAF in routine clinical care in the Republic of Korea, Singapore, and Taiwan. Endpoints at month 24 included effectiveness (HIV-1 RNA <50 copies/mL; missing = excluded and discontinuation = failure analyses), immunological endpoints (CD4 cell count and CD4/CD8 ratio), persistence, safety, and patient-reported outcomes (prospective cohort). Overall, 334 participants (252 prospective, 82 retrospective; 66 TN, 268 TE) were included in the analysis population. Most were male (97% TN, 93% TE) with ≥1 comorbidity (56% TN, 67% TE). At month 24, HIV-1 RNA was <50 copies/mL in 91% (50/55) of TN and 97% (225/331) of TE participants (missing = excluded analysis). Median (quartile [Q]1, Q3) CD4 count increased by +260 (155, 386; P < .001) cells/μL in TN and +40 (-65, 150; P = .008) cells/μL in TE participants. Median (Q1, Q3) CD4/CD8 ratio increased by +0.38 (0.21, 0.48; P < .001) in TN and +0.08 (0.00, 0.19; P < .001) in TE participants. Patient-reported outcomes indicated an improvement in mental health and a decrease in the number of bothersome symptoms in TN participants. Persistence at month 24 was high, with 98% (60/61) of TN and 97% (251/260) of TE participants remaining on B/F/TAF. Drug-related adverse events occurred in 9% (6/66) of TN and 8% (22/268) of TE participants, leading to B/F/TAF discontinuation in <1% (3/334) of participants, all of whom were TE. B/F/TAF demonstrated high levels of effectiveness, persistence, and tolerability over 24 months in people with HIV in Asia.

INTRODUCTION:Guidelines advocate the treatment of HCV in all HIV/HCV co-infected individuals. The aim of this randomized, open-label study (ClinicalTrials.gov identifier: NCT02707601; https://clinicaltrials.gov/ct2/show/NCT02707601) was to evaluate the safety/efficacy of ledipasvir/sofosbuvir (LDV/SOF) co-administered with elvitegravir/cobicistat/emtricitabine/tenofovir alafenamide (E/C/F/TAF) or rilpivirine/F/TAF (R/F/TAF) in HIV-1/HCV co-infected participants.METHODS:Participants with HIV-1 RNA <50 copies/mL and chronic HCV-genotype (GT) 1 (HCV treatment-naïve ± compensated cirrhosis or HCV treatment-experienced non-cirrhotic) were randomized 1:1 to switch to E/C/F/TAF or R/F/TAF. If HIV suppression was maintained at Week 8, participants received 12 weeks of LDV/SOF. The primary endpoint was sustained HCV virologic response 12 weeks after LDV/SOF completion (SVR12).RESULTS:Of 150 participants, 148 received ≥1 dose of HIV study drug and 144 received LDV/SOF (72 in each F/TAF group; 83% GT1a, 94% HCV treatment-naïve, 12% cirrhotic). Overall, SVR12 was 97% (95% confidence interval: 93-99%). Black race did not affect SVR12. Of four participants not achieving SVR12, one had HCV relapse, one had HCV virologic non-response due to non-adherence, and two missed the post-HCV Week 12 visit. Of 148 participants, 96% receiving E/C/F/TAF and 95% receiving R/F/TAF maintained HIV suppression at Week 24; no HIV resistance was detected. No participant discontinued LDV/SOF or E/C/F/TAF due to adverse events; one participant discontinued R/F/TAF due to worsening of pre-existing hypercholesterolemia. Renal toxicity was not observed in either F/TAF regimen during LDV/SOF co-administration. In conclusion, high rates of HCV SVR12 and maintenance of HIV suppression were achieved with LDV/SOF and F/TAF-based regimens.CONCLUSION:This study supports LDV/SOF co-administered with an F/TAF-based regimen in HIV-1/HCV-GT1 co-infected patients.

Antiretroviral therapies have proved life‐saving in HIV infection, dramatically reducing morbidity and mortality. With longer survival, morbidities and mortalities in HIV infection are increasingly similar to the morbidities and mortalities associated with ageing. In treated HIV infection, the risk of these morbidities and mortalities is linked to immune activation, inflammation and coagulation indices. And in persons with treated HIV infection, failure to restore circulating CD4 T cell numbers is associated with a greater risk of morbidities and mortalities as well as to heightened levels of inflammation and coagulation. The drivers of immune activation, inflammation and coagulation in treated HIV infection are incompletely defined and could be related to sustained low levels of viral replication in tissues, to translocation of microbial products across a damaged gut mucosa, to replication of co‐pathogens such as cytomegalovirus, to increased levels of inflammatory lipids, or to homeostatic responses to lymphocytopenia that may drive expansion of CD8 T cell numbers. We present here models that link inflammation and coagulation to morbid outcomes as well as to the pathogenesis of CD4 T cell restoration failure and CD8 T cell expansion.

Antiretroviral therapies have proved life-saving in HIV infection, dramatically reducing morbidity and mortality.With longer survival, morbidities and mortalities in HIV infection are increasingly similar to the morbidities and mortalities associated with ageing.In treated HIV infection, the risk of these morbidities and mortalities is linked to immune activation, inflammation and coagulation indices.And in persons with treated HIV infection, failure to restore circulating CD4 T cell numbers is associated with a greater risk of morbidities and mortalities as well as to heightened levels of inflammation and coagulation.The drivers of immune activation, inflammation and coagulation in treated HIV infection are incompletely defined and could be related to sustained low levels of viral replication in tissues, to translocation of microbial products across a damaged gut mucosa, to replication of co-pathogens such as cytomegalovirus, to increased levels of inflammatory lipids, or to homeostatic responses to lymphocytopenia that may drive expansion of CD8 T cell numbers.We present here models that link inflammation and coagulation to morbid outcomes as well as to the pathogenesis of CD4 T cell restoration failure and CD8 T cell expansion.

Antiretroviral therapies have proved life-saving in HIV infection, dramatically reducing morbidity and mortality.With longer survival, morbidities and mortalities in HIV infection are increasingly similar to the morbidities and mortalities associated with ageing.In treated HIV infection, the risk of these morbidities and mortalities is linked to immune activation, inflammation and coagulation indices.And in persons with treated HIV infection, failure to restore circulating CD4 T cell numbers is associated with a greater risk of morbidities and mortalities as well as to heightened levels of inflammation and coagulation.The drivers of immune activation, inflammation and coagulation in treated HIV infection are incompletely defined and could be related to sustained low levels of viral replication in tissues, to translocation of microbial products across a damaged gut mucosa, to replication of co-pathogens such as cytomegalovirus, to increased levels of inflammatory lipids, or to homeostatic responses to lymphocytopenia that may drive expansion of CD8 T cell numbers.We present here models that link inflammation and coagulation to morbid outcomes as well as to the pathogenesis of CD4 T cell restoration failure and CD8 T cell expansion.