Prognostic Value of Serum HIV-RNA Levels at Virologic Steady State After Seroconversion: Relation to CD4 Cell Count and Clinical Course of Primary Infection

Author(s):  
Court Pedersen ◽  
Therese Katzenstein ◽  
Claus Nielsen ◽  
Jens D. Lundgren ◽  
Jan Gerstoft
AIDS ◽  
2010 ◽  
Vol 24 (10) ◽  
pp. 1561-1567 ◽  
Author(s):  
Andrew N Phillips ◽  
Fiona C Lampe ◽  
Colette J Smith ◽  
Anna-Maria Geretti ◽  
Alison Rodger ◽  
...  

2017 ◽  
Vol 11 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Miyuki Kawado ◽  
Shuji Hashimoto ◽  
Shin-ichi Oka ◽  
Katsuyuki Fukutake ◽  
Satoshi Higasa ◽  
...  

Objective: This study aimed to determine improvement in HIV RNA levels and the CD4 cell count by switching to an antiretroviral regimen with an integrase strand transfer inhibitor (INSTI) in patients with HIV. Method: This study was conducted on Japanese patients with HIV who were infected by blood products in the 1980s. Data were collected between 2007 and 2014. Data of 564 male hemophiliac patients with HIV from the Japan Cohort Study of HIV Patients Infected through Blood Products were available. Changes in antiretroviral regimen use, HIV RNA levels, and the CD4 cell count between 2007 and 2014 were examined. Results: From 2007 to 2014, the proportion of use of a regimen with an INSTI increased from 0.0% to 41.0%. For patients with HIV who used a regimen, including an INSTI, the proportion of HIV RNA levels <50 copies/mL significantly increased from 58.3% in 2007 to 90.6% in 2014. Additionally, the median CD4 cell count significantly increased from 380/μL to 438/μL. Conclusion: There is a large effect of switching to an antiretroviral regimen with an INSTI for Japanese patients with HIV who are infected by blood products. This suggests that performing this switch in clinical practice will lead to favorable effects.


AIDS ◽  
1999 ◽  
Vol 13 (6) ◽  
pp. F35-F43 ◽  
Author(s):  
Steven G. Deeks ◽  
Frederick M. Hecht ◽  
Melinda Swanson ◽  
Tarek Elbeik ◽  
Richard Loftus ◽  
...  

2005 ◽  
Vol 16 (3) ◽  
pp. 243-246 ◽  
Author(s):  
Somnuek Sungkanuparph ◽  
Sasisopin Kiertiburanakul ◽  
Weerawat Manosuthi ◽  
Wiphawee Kiatatchasai ◽  
Asda Vibhagool

In developing countries, patients often present late with advanced AIDS and a very low CD4 cell count. A retrospective cohort study was conducted in HIV-infected patients who had been initiated into highly active antiretroviral therapy (HAART) with CD4 cell count <50 cells/mm3. There were 159 patients of mean age 36.6 years and 60.4% had previous major opportunistic infections. Mean CD4 was 22 cells/mm3 and 80% had HIV RNA>100,000 copies/mL. The majority of HAART regimens is non-nucleoside reverse transcriptase inhibitor-based (81.8%). In as-treated analysis, 50, 71.2, 79.7, 79.4, and 80.1% of patients achieved undetectable HIV RNA (<50 copies/mL) at 12, 24, 36, 48, and 60 weeks, respectively. The corresponding mean CD4 counts were 95, 125, 166, 201, and 225 cells/mm3. Twenty two patients (13.8%) had adverse drug events and half of these had to discontinue HAART. Initiation of HAART in advanced AIDS with CD4 cell count <50 cells/mm3 is effective, safe, and well tolerated and should not be delayed.


2008 ◽  
Vol 42 (5) ◽  
pp. 621-626 ◽  
Author(s):  
Parya Saberi ◽  
Nikolai H Caswell ◽  
Cristina I Gruta ◽  
Jason N Tokumoto ◽  
Betty J Dong

Background: Randomized clinical trials have demonstrated that enfuvirtide plus an optimized background regimen can cause a significant increase in CD4+ cell counts and a reduction in HIV RNA levels. Objective: To describe and anaiyze CD4+ cell count and HIV RNA changes in HIV-infected patients receiving enfuvirtide and a prescribed background regimen (PBR) in a primarily clinical setting. Methods: A retrospective review from September 1998 through August 2005 of CD4+ cell counts and HIV RNA changes from baseline was conducted in patients receiving enfuvirtide. Data were stratified and analyzed according to baseline CD4+ cell count and HIV RNA. Results: A mean CD4+ cell count increase of approximately 102 cells/mm3 was observed, regardless of baseline CD4+ cell count, in 187 patients receiving enfuvirtide during a mean of 19.4 months of follow-up. During 3 years of follow-up, patients initiating enfuvirtide at CD4+ cell counts less than 100 cells/mm3 never achieved absolute CD4+ cell counts comparable to the counts in patients starting enfuvirtide at CD4+ cell counts of 100 cells/mm3 or more. In 38.3% of patients achieving an undetectable HIV RNA level, a mean CD4+ cell count increase of 185 cells/mm3 was observed. An unexpected finding was that a mean CD4+ cell count increase of 76 cells/mm3 occurred in 61.7% of patients not achieving complete viral suppression. Conclusions: Immunologic benefits were observed in subjects continuing enfuvirtide plus a PBR irrespective of baseline CD4+ cell count, complete viral suppression, or antiretroviral susceptibility data. Dala suggest that initiation of enfuvirtide at CD4+ cell counts greater than 100 celis/mm3 may be immunologically advantageous and independent of complete virologic response.


2016 ◽  
Vol 29 (4) ◽  
pp. 859-880 ◽  
Author(s):  
Véronique Avettand-Fènoël ◽  
Laurent Hocqueloux ◽  
Jade Ghosn ◽  
Antoine Cheret ◽  
Pierre Frange ◽  
...  

SUMMARYHIV-1 DNA persists in infected cells despite combined antiretroviral therapy (cART), forming viral reservoirs. Recent trials of strategies targeting latent HIV reservoirs have rekindled hopes of curing HIV infection, and reliable markers are thus needed to evaluate viral reservoirs. Total HIV DNA quantification is simple, standardized, sensitive, and reproducible. Total HIV DNA load influences the course of the infection and is therefore clinically relevant. In particular, it is predictive of progression to AIDS and death, independently of HIV RNA load and the CD4 cell count. Baseline total HIV DNA load is predictive of the response to cART. It declines during cART but remains quantifiable, at a level that reflects both the history of infection (HIV RNA zenith, CD4 cell count nadir) and treatment efficacy (residual viremia, cumulative viremia, immune restoration, immune cell activation). Total HIV DNA load in blood is also predictive of the presence and severity of some HIV-1-associated end-organ disorders. It can be useful to guide individual treatment, notably, therapeutic de-escalation. Although it does not distinguish between replication-competent and -defective latent viruses, the total HIV DNA load in blood, tissues, and cells provides insights into HIV pathogenesis, probably because all viral forms participate in host cell activation and HIV pathogenesis. Total HIV DNA is thus a biomarker of HIV reservoirs, which can be defined as all infected cells and tissues containing all forms of HIV persistence that participate in pathogenesis. This participation may occur through the production of new virions, creating new cycles of infection and disseminating infected cells; maintenance or amplification of reservoirs by homeostatic cell proliferation; and viral transcription and synthesis of viral proteins without new virion production. These proteins can induce immune activation, thus participating in the vicious circle of HIV pathogenesis.


2019 ◽  
Vol 6 (2) ◽  
Author(s):  
Oskar Olsson ◽  
Per Björkman ◽  
Marianne Jansson ◽  
Taye Tolera Balcha ◽  
Daba Mulleta ◽  
...  

Abstract Background Diagnosis of tuberculosis (TB) in human immunodeficiency virus (HIV)-coinfected individuals is challenging. We hypothesized that combinations of inflammatory markers could facilitate identification of active TB in HIV-positive individuals. Methods Participants were HIV-positive, treatment-naive adults systematically investigated for TB at Ethiopian health centers. Plasma samples from 130 subjects with TB (HIV+/TB+) and 130 subjects without TB (HIV+/TB−) were tested for concentration of the following markers: CCL5, C-reactive protein (CRP), interleukin (IL)-6, IL12-p70, IL-18, IL-27, interferon-γ-induced protein-10 (IP-10), procalcitonin (PCT), and soluble urokinase-type plasminogen activator receptor (suPAR). Analyzed markers were then assessed, either individually or in combination, with regard to infection status, CD4 cell count, and HIV ribonucleic acid (RNA) levels. Results The HIV+/TB+ subjects had higher levels of all markers, except IL12p70, compared with HIV+/TB− subjects. The CRP showed the best performance for TB identification (median 27.9 vs 1.8 mg/L for HIV+/TB+ and HIV+/TB−, respectively; area under the curve [AUC]: 0.80). Performance was increased when CRP was combined with suPAR analysis (AUC, 0.83 [0.93 for subjects with CD4 cell count &lt;200 cells/mm3]). Irrespective of TB status, IP-10 concentrations correlated with HIV RNA levels, and both IP-10 and IL-18 were inversely correlated to CD4 cell counts. Conclusions Although CRP showed the best single marker discriminatory potential, combining CRP and suPAR analyses increased performance for TB identification.


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