scholarly journals Effective Human Immunodeficiency Virus Molecular Surveillance Requires Identification of Incident Cases of Infection

Author(s):  
Susan J Little ◽  
Tom Chen ◽  
Rui Wang ◽  
Christy Anderson ◽  
Sergei Kosakovsky Pond ◽  
...  

Abstract Background Ending the human immunodeficiency virus (HIV) epidemic requires knowledge of key drivers of spread of HIV infection. Methods Between 1996 and 2018, 1119 newly and previously diagnosed, therapy-naive persons with HIV (PWH) from San Diego were followed. A genetic distance–based network was inferred using pol sequences, and genetic clusters grew over time through linkage of sequences from newly observed infections. Cox proportional hazards models were used to identify factors associated with the rate of growth. These results were used to predict the impact of a hypothetical intervention targeting PWH with incident infection. Comparison was made to the Centers for Disease Control and Prevention (CDC) Ending the HIV Epidemic (EHE) molecular surveillance strategy, which prioritizes clusters recently linked to all new HIV diagnoses and does not incorporate data on incident infections. Results Overall, 219 genetic linkages to incident infections were identified over a median follow-up of 8.8 years. Incident cluster growth was strongly associated with proportion of PWH in the cluster who themselves had incident infection (hazard ratio, 44.09 [95% confidence interval, 17.09–113.78]). The CDC EHE molecular surveillance strategy identified 11 linkages to incident infections a genetic distance threshold of 0.5%, and 24 linkages at 1.5%. Conclusions Over the past 2 decades, incident infections drove incident HIV cluster growth in San Diego. The current CDC EHE molecular detection and response strategy would not have identified most transmission events arising from those with incident infection in San Diego. Molecular surveillance that includes detection of incident cases will provide a more effective strategy for EHE.

1989 ◽  
Vol 29 (3) ◽  
pp. 181-185 ◽  
Author(s):  
David M. Novick ◽  
Harold L. Trigg ◽  
Don C. Des Jarlais ◽  
Samuel R. Friedman ◽  
David Vlahov ◽  
...  

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Vegard Eldholm ◽  
Adrien Rieux ◽  
Johana Monteserin ◽  
Julia Montana Lopez ◽  
Domingo Palmero ◽  
...  

The tuberculosis (TB) epidemic is fueled by a parallel Human Immunodeficiency Virus (HIV) epidemic, but it remains unclear to what extent the HIV epidemic has been a driver for drug resistance in Mycobacterium tuberculosis (Mtb). Here we assess the impact of HIV co-infection on the emergence of resistance and transmission of Mtb in the largest outbreak of multidrug-resistant TB in South America to date. By combining Bayesian evolutionary analyses and the reconstruction of transmission networks utilizing a new model optimized for TB, we find that HIV co-infection does not significantly affect the transmissibility or the mutation rate of Mtb within patients and was not associated with increased emergence of resistance within patients. Our results indicate that the HIV epidemic serves as an amplifier of TB outbreaks by providing a reservoir of susceptible hosts, but that HIV co-infection is not a direct driver for the emergence and transmission of resistant strains.


1996 ◽  
Vol 168 (S30) ◽  
pp. 117-122 ◽  
Author(s):  
Mario Maj

The association between the infection produced by the human immunodeficiency virus (HIV) and syndromal or subsyndromal depression has been the topic of several studies in recent years. The results of the WHO Neuropsychiatric AIDS Study, conducted in the five geographical areas predominantly affected by the HIV epidemic, suggest that the symptomatic stages of HIV infection are associated with an increased prevalence of depressive symptoms, and, at least in some contexts in which the spreading of the infection is more recent and the social rejection of HIV-seropositive subjects is harsher, may also be associated with an increased prevalence of a syndromal diagnosis of depression.


1989 ◽  
Vol 13 (1-2) ◽  
pp. 13-37
Author(s):  
Richard H. Needle ◽  
Susan Leach ◽  
Robin P. Graham-Tomasi

1990 ◽  
Vol 11 (8) ◽  
pp. 419-421 ◽  

These surveys continue to serve as a glimpse of public health laboratory activities at a point just prior to a Consensus Conference. Generally, the surveys offer some benefit to Consensus Conference deliberations by providing data for emerging issues or identifying problems not previously thought to be an issue.Response to the surveys continues to fall short of replies from all 54 states and territories. Each has its own reason for not responding, but it would be nice if someday the response was 100%. Figure 1 shows that responses were received from 42 states, one territory and one city. The fact that states with significant involvement in the human immunodeficiency virus (HIV) epidemic did not respond greatly reduces the overall value of this survey, but the limited data must suffice.


2003 ◽  
Vol 77 (3) ◽  
pp. 1940-1950 ◽  
Author(s):  
Jennifer M. Babik ◽  
Mark Holodniy

ABSTRACT This study analyzes the effect of highly active antiretroviral therapy (HAART), and thus immunologic status, on hepatitis C virus (HCV) load and quasispecies diversity in patients coinfected with the human immunodeficiency virus (HIV) and HCV. Three cohorts of coinfected patients were analyzed retrospectively over a period of 7 to 10 months: group A was antiretroviral drug naïve at baseline and then on HAART for the remainder of the study, group B did not receive antiretroviral therapy at any point, and group C was on HAART for the entire study. HCV quasispecies diversity was analyzed by sequencing hypervariable region 1. In a longitudinal analysis, there was no significant change from baseline in any immunologic, virologic, or quasispecies parameter in any of the three groups. However, in comparison to groups A and B, group C had significantly higher CD4+- and CD8+-cell counts, a trend toward a higher HCV load, and significantly increased number of HCV clones, entropy, genetic distance, and ratio of nonsynonymous substitutions per nonsynonymous site to synonymous substitutions per synonymous site (Ka /Ks ). In addition, CD4+-cell count was positively correlated with HCV load, genetic distance, and Ka . Interestingly, patients infected with HCV genotype 2 or 3 had a significantly higher CD4+-cell count, HCV load, genetic distance, and Ka /Ks than those infected with genotype 1. These results suggest that there is no immediate effect of HAART on HCV but that, with prolonged HAART, immune restoration results in an increase in HCV load and quasispecies diversity.


Author(s):  
Bram Vrancken ◽  
Sanjay R Mehta ◽  
Santiago Ávila-Ríos ◽  
Claudia García-Morales ◽  
Daniela Tapia-Trejo ◽  
...  

Abstract Background Evolutionary analyses of well-annotated human immunodeficiency virus (HIV) sequence data can provide insights into viral transmission patterns and associated factors. Here, we explored the transmission dynamics of the HIV-1 subtype B epidemic across the San Diego (US) and Tijuana (Mexico) border region to identify factors that could help guide public health policy. Methods HIV pol sequences were collected from people with HIV in San Diego County and Tijuana between 1996–2018. A multistep phylogenetic approach was used to characterize the dynamics of spread. The contributions of geospatial factors and HIV risk group to the local dynamics were evaluated. Results Phylogeographic analyses of the 2034 sequences revealed an important contribution of local transmission in sustaining the epidemic, as well as a complex viral migration network across the region. Geospatial viral dispersal between San Diego communities occurred predominantly among men who have sex with men, with central San Diego being the main source (34.9%) and recipient (39.5%) of migration events. HIV migration was more frequent from San Diego county towards Tijuana than vice versa. Migrations were best explained by the driving time between locations. Conclusions The US-Mexico border may not be a major barrier to the spread of HIV, which may stimulate coordinated transnational intervention approaches. Whereas a focus on central San Diego has the potential to avert most spread, the substantial viral migration independent of central San Diego shows that county-wide efforts will be more effective. Combined, this work shows that epidemiological information gleaned from pathogen genomes can uncover mechanisms that underlie sustained spread and, in turn, can be a building block of public health decision-making.


2016 ◽  
Vol 3 (3) ◽  
Author(s):  
Saran Vardhanabhuti ◽  
David Katzenstein ◽  
John Bartlett ◽  
Nagalingeswaran Kumarasamy ◽  
Carole L. Wallis

Abstract Background.  The mechanism of virologic failure (VF) of lopinavir/ritonavir (LPV/r) monotherapy is not well understood. We assessed sequence changes in human immunodeficiency virus-1 reverse-transcriptase (RT) and protease (PR) regions. Methods.  Human immunodeficiency virus-1 pol sequences from 34 participants who failed second-line LPV/r monotherapy were obtained at study entry (SE) and VF. Sequence changes were evaluated using phylogenetic analysis and hamming distance. Results.  Human immunodeficiency virus-1 sequence change was higher over drug resistance mutation (DRM) sites (median genetic distance, 2.2%; Q1 to Q3, 2.1%–2.5%) from SE to VF compared with non-DRM sites (median genetic distance, 1.3%; Q1 to Q3, 1.0%–1.4%; P < .0001). Evolution over DRM sites was mainly driven by changes in the RT (median genetic distance, 2.7%; Q1 to Q3, 2.2%–3.2%) compared with PR (median genetic distance, 1.1%; Q1 to Q3, 0.0%–1.1%; P < .0001). Most RT DRMs present at SE were lost at VF. At VF, 19 (56%) and 26 (76%) were susceptible to efavirenz/nevirapine and etravirine (ETV)/rilpivirine (RPV), respectively, compared with 1 (3%) and 12 (35%) at SE. Participants who retained nonnucleoside reverse-transcriptase inhibitor (NNRTI) DRMs and those without evolution of LPV/r DRMs had significantly shorter time to VF. Conclusions.  The selection of LPV/r DRMs in participants with longer time to VF suggests better adherence and more selective pressure. Fading NNRTI mutations and an increase in genotypic susceptibility to ETV and RPV could allow for the reuse of NNRTI. Further studies are warranted to understand mechanisms of PR failure.


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