Characterizing Patients with Very-Low-Level HIV Viremia: A Community-Based Study

Abstract

Objective: Very-low-level viremia (VLLV) is a relatively new concept in the realm of human immunodeficiency virus (HIV) care. Newer generation assays are now able to detect plasma HIV RNA Viral Load (VL) levels as low as 20 copies/mL. The authors characterized patients with VLLV (VL between 20 and 50 copies/mL) in order to identify possible risk factors associated with virologic failure and poor clinical outcomes. Methods: The authors reviewed 119 consecutive charts of patients with VLLV. Sociodemographic data were extracted and viral load and CD4 counts were trended over a 12 month period (February 2013-February 2014. Regression analysis was used to assess the role of different factors on virologic failure at 1 year. Results: Of the study participants with evaluable data (n ¼ 100), the median age was 53 years (interquartile range: 43-57.5), 67% were nonwhite, 34% were women, 58% were smokers, 47% were alcoholics, 58% had a history of intravenous drug use, and 40% were coinfected with hepatitis C virus. More than half of the participants had 3 or more comorbidities and their HIV pill burden was high (more than 2 pills daily). After 12 months, 65 participants achieved undetectable viral load levels, whereas 15 experienced virologic failure (2 consecutive viral loads > 50 copies/mL) and the remaining 20 had persistent VLLV. In the virologic failure group, there was a predominance of white males (66%) with a significant number of comorbidities and pill burden. Univariate logistic regression suggested that there was a difference between the failure versus nonfailure groups in terms of race, ethnicity, and alcohol use. Multivariate regression with virological failure as the outcome suggested a trend only in terms of participant's alcohol use. Conclusion: Most patients with initial VLLV (70%) achieved virologic suppression at 1 year with no antiretroviral therapy changes. Thus, VLLV does not necessarily predict virologic failure and should not prompt more frequent clinic visits or antiretroviral regimen changes. Further research is needed in order to determine the predictors of virologic failure in this subset of patients and the clinicians' attitude toward VLLV.

INSTI-Based Triple Regimens in Treatment-Naïve HIV-Infected Patients Are Associated With HIV-RNA Viral Load Suppression at Ultralow Levels

“…Past research has shown that patients with a slower time to achieving <50 copies/mL are more likely to continue treatment with residual viremia [13], and when <50 copies/mL occurs >6 months after initiating ART, they have an almost 2-fold risk of subsequent VR [6]. Reports with clearer evidence have stated that the inability to achieve UL-VL during firstline therapy could lead to a higher risk of VR in certain settings [33, 34], whereas others failed to observe similar results [35]. In our study, we observed that patients without VR were able to suppress UL-VL not detected at a significantly faster rate, similar to patients with “high” suppression of UL HIV-RNA during the course of treatment.…”

Human immunodeficiency virus and hepatotropic viruses co-morbidities as the inducers of liver injury progression

“…As reported, ART delays the progression to cirrhosis in HIV/HCV co-infection[90,91]. Patients with undetectable or low levels of HIV RNA tend to develop liver disease gradually compared to patients with detectable viremia[92,93]. Furthermore, HIV treatment reduces the complications of the end-stage liver diseases, such as hepatocellular carcinoma (HCC) and death[94-96].…”

Impacto de la viremia de bajo grado en el riesgo de fallo virológico en pacientes con infección por VIH-1

“…Los estudios publicados hasta el presente han demostrado hallazgos contradictorios en relación con la presencia de CVBG y el riesgo posterior de FV. Algunas publicaciones han observado que la presencia de CVBG es frecuente y que no se asocia con el desarrollo posterior de FV 5,9 . Otros estudios mostraron que los pacientes con CVBG tuvieron mayor riesgo de evolucionar a FV que los pacientes que se mantuvieron persistentemente indetectables 4,6,7 .…”

“…Los autores consideraron que los factores que contribuyeron a la presencia de CVBG intermitente o permanente podrían ser la existencia de reservorios virales, variaciones o error de laboratorio, continua replicación viral en tejidos y disminución de la adherencia. La CVBG por períodos prolongados podría estar asociada a activación inmune, aunque no se puede predecir el impacto clínico que conlleva 5 .…”