Suspected HIV drug resistance linked to raised inflammation and altered clotting in Kenya

Adults living with HIV at Kisii Teaching and Referral Hospital in Kenya who were suspected of having developed resistance to highly active antiretroviral therapy showed markedly higher levels of C-reactive protein and longer clotting times than patients whose treatment was still considered effective, according to a comparative cross-sectional study published in BMC Infectious Diseases.

The study enrolled HIV-positive adults at the hospital and divided them into two groups based on viral load: those suspected of HAART resistance and those regarded as HAART-susceptible. Participants were recruited through systematic random sampling, and venous blood samples from each group were analysed for C-reactive protein, a marker of systemic inflammation, and for two standard measures of blood clotting, prothrombin time and activated partial thromboplastin time.

The researchers, led by Elina Moige with Paul Kosiyo and Collins Ouma, compared the three markers between the two groups using the Mann-Whitney U test. C-reactive protein levels were significantly higher among the suspected HAART-resistant patients than among the HAART-susceptible patients, a difference the authors reported as statistically significant with a p value of 0.01.

Both clotting measures also differed between the groups. Prothrombin time was higher in the suspected resistant group, with a p value of 0.002, and activated partial thromboplastin time was likewise higher, with a p value of 0.011.

To examine how the markers related to suspected resistance, the team used binary logistic regression. C-reactive protein was associated with suspected HAART resistance, with an odds ratio of 1.051, a 95 percent confidence interval of 1.025 to 1.078, and a p value of 0.001. Because the odds ratio is close to one, this reflects a modest increase in odds per unit rise in the inflammatory marker rather than a large effect.

The study also assessed the relationship between inflammation and clotting directly. C-reactive protein correlated positively with prothrombin time, with a correlation coefficient of 0.339 and a p value of 0.001, and with activated partial thromboplastin time, with a coefficient of 0.305 and a p value of 0.001, across the suspected resistant and susceptible groups respectively. These positive correlations indicate that higher levels of the inflammatory marker tended to accompany longer clotting times in this cohort.

Interpreting the pattern, the authors concluded that suspected HAART-resistant HIV-positive patients in the study had elevated C-reactive protein together with prolonged prothrombin and activated partial thromboplastin times, which they suggest points to persistent immune activation and an inflammatory-coagulation process. They argue that this combination supports the need for early detection of inflammatory and coagulation dysregulation among patients suspected of treatment resistance, even while they remain on continuous medication.

The clinical background for the work is that HIV-infected patients may develop treatment resistance associated with persistent inflammation and coagulation abnormalities despite antiretroviral therapy. The authors note that data on these markers among suspected HAART-resistant patients in Kisii County had been limited, hindering evidence-based monitoring of thrombotic complications, which motivated the study’s focus on comparing these specific markers between the two patient groups.

Several features of the study design shape how the findings should be read. The work is a comparative cross-sectional analysis of patients at a single Kenyan hospital, categorised by viral load as suspected resistant or susceptible, so it captures associations at one point in time rather than tracking changes within individuals. The reported differences and correlations describe this enrolled cohort, and the regression association between C-reactive protein and suspected resistance is a statistical association rather than evidence that inflammation causes resistance or that resistance causes clotting abnormalities. The authors describe the study as identifying a need for monitoring, and the findings apply to the suspected HAART-resistant and HAART-susceptible adults studied at Kisii Teaching and Referral Hospital.

Within those limits, the study adds local data to a question of practical importance for HIV care in the region: whether routinely measurable inflammatory and coagulation markers can help flag patients whose antiretroviral regimen may be failing. The results indicate that in this Kenyan cohort, suspected treatment resistance was accompanied by higher C-reactive protein and longer prothrombin and activated partial thromboplastin times, and that the inflammatory and clotting measures moved together, supporting the authors’ call for closer attention to these markers in patients with suspected HAART resistance.

Subject of Research: Inflammatory and coagulation markers in HIV patients with suspected antiretroviral therapy resistance in Kenya

Article Title: Inflammatory markers and coagulation profile among HIV patients with suspected highly active antiretroviral therapy resistance in Kisii Teaching and Referral Hospital, Kenya

Article References: Moige, E., Kosiyo, P., & Ouma, C. (2026). Inflammatory markers and coagulation profile among HIV patients with suspected highly active antiretroviral therapy resistance in Kisii Teaching and Referral Hospital, Kenya. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14415-y

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14415-y

Keywords: HIV, antiretroviral therapy resistance, C-reactive protein, prothrombin time, activated partial thromboplastin time, coagulation, inflammation, viral load, Kenya, cross-sectional study, BMC Infectious Diseases, Inflammatory