Baseline characteristics of the 987 patients from the ANRS PRIMO cohort 1999–2010.

<p>TPHA = <i>Treponema palladium</i> haemagglutination assay; VDRL = Venereal Diseases Research Laboratory test; HBV = hepatits B virus; HCV = hepatitis C virus.</p

Comparison of the characteristics of patients included into clustered transmission versus non-clustered: the ANRS PRIMO cohort 1999–2010.

<p>Note: the total of patients for each variable does not always equal the total sample due to some missing values. PHI = primary HIV infection; MSM = men having sex with men; TPHA = <i>Treponema palladium</i> haemagglutination assay; VDRL = Venereal Diseases Research Laboratory test.</p>(1)<p>Urethritis, rectitis, genital herpes infection, vulvo-vaginal candidosis, condyloma and/or syphilis.</p>(2)<p>In the last 6 months preceding PHI diagnosis.</p

Comparative <i>Highlighter</i> analyses of <i>env</i> diversity in a donor-recipient HIV-1 transmission pair.

<p>(A) Recipient#1 shows evidence of infection with a single virus. (B) Donor#1 was the chronically infected partner of recipient#1. The same reference amplicon, a V3 RNA sequence from recipient plasma, was used to depict the viral diversity in both individuals.</p

Characteritics of the 8 donors.

¶<p>Results based on the declaration of the recipient.</p><p>EIA-RI test = enzyme-linked immunosorbent assay for recent infection <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0069144#pone.0069144-Barin1" target="_blank">[29]</a>, PBMC = peripheral blood mononuclear cells; Het = heterosexual; MSM = man having sex with men; HBV = hepatits B virus; HBsAg = HBV surface antigen; HBsAb = HBV surface antibodies; HBcAb = HBV core antibodies; HCV = hepatitis C virus; n.d. = not done; n.a. = data not available; und = undetectable.</p

Evolutionary relationships between the HIV-1 <i>env</i> genes in the eight donor/recipient pairs.

<p>The evolutionary history was inferred using the Neighbor-Joining method <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0069144#pone.0069144-Boeras1" target="_blank">[38]</a>. The optimal tree with the sum of branch length = 2.01912678 is shown. The tree is drawn to scale, with branch length in the same units as those of the evolutionary distances used to infer the phylogenetic tree. The evolutionary distances were computed using the Maximum Composite Likelihood method <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0069144#pone.0069144-Whitney1" target="_blank">[39]</a> and the unit is the number of base substitutions per site. Codon positions included were 1^st+2^nd+3^rd+noncoding. All positions containing gaps and missing data were eliminated from the dataset. There were a total of 230 positions in the final dataset. Phylogenetic analyses were conducted in MEGA4 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0069144#pone.0069144-Redd1" target="_blank">[40]</a>. For each recipient, viruses isolated from PBMC-derived DNA (•) and plasma RNA (○) are represented, with a different color for each donor/recipient pair. Asterisks indicate branches with bootstrap values greater than 98%.</p

Characteritics of the 8 recipients.

*<p>In the 6 months preceding PHI diagnosis.</p>§<p>Urethritis, rectitis, genital herpes infection, vulvo-vaginal candidosis, condyloma and/or syphilis.</p><p>PBMC = peripheral blood mononuclear cells; Het = heterosexual; MSM = man having sex with men; HBV = hepatits B virus; HBsAg = HBV surface antigen; HBsAb = HBV surface antibodies; HBcAb = HBV core antibodies; HCV = hepatitis C virus; n.d. = not done; und = undetectable.</p

image_5_Mass Cytometry Analysis Reveals the Landscape and Dynamics of CD32a+ CD4+ T Cells From Early HIV Infection to Effective cART.PDF

<p>CD32a has been proposed as a specific marker of latently HIV-infected CD4⁺ T cells. However, CD32a was recently found to be expressed on CD4⁺ T cells of healthy donors, leading to controversy on the relevance of this marker in HIV persistence. Here, we used mass cytometry to characterize the landscape and variation in the abundance of CD32a⁺ CD4⁺ T cells during HIV infection. To this end, we analyzed CD32a⁺ CD4⁺ T cells in primary HIV infection before and after effective combination antiretroviral therapy (cART) and in healthy donors. We found that CD32a⁺ CD4⁺ T cells include heterogeneous subsets that are differentially affected by HIV infection. Our analysis revealed that naive (_N), central memory (_CM), and effector/memory (_Eff/Mem) CD32a⁺ CD4⁺ T-cell clusters that co-express LILRA2- and CD64-activating receptors were more abundant in primary HIV infection and cART stages. Conversely, LILRA2⁻ CD32a⁺ CD4⁺ T-cell clusters of either the T_N, T_CM, or T_Eff/Mem phenotype were more abundant in healthy individuals. Finally, an activated CD32a⁺ CD4⁺ T_Eff/Mem cell cluster co-expressing LILRA2, CD57, and NKG2C was more abundant in all HIV stages, particularly during primary HIV infection. Overall, our data show that multiple abundance modifications of CD32a⁺ CD4⁺ T-cell subsets occur in the early phase of HIV infection, and some of which are conserved after effective cART. Our study brings a better comprehension of the relationship between CD32a expression and CD4⁺ T cells during HIV infection.</p

image_2_Mass Cytometry Analysis Reveals the Landscape and Dynamics of CD32a+ CD4+ T Cells From Early HIV Infection to Effective cART.PDF

<p>CD32a has been proposed as a specific marker of latently HIV-infected CD4⁺ T cells. However, CD32a was recently found to be expressed on CD4⁺ T cells of healthy donors, leading to controversy on the relevance of this marker in HIV persistence. Here, we used mass cytometry to characterize the landscape and variation in the abundance of CD32a⁺ CD4⁺ T cells during HIV infection. To this end, we analyzed CD32a⁺ CD4⁺ T cells in primary HIV infection before and after effective combination antiretroviral therapy (cART) and in healthy donors. We found that CD32a⁺ CD4⁺ T cells include heterogeneous subsets that are differentially affected by HIV infection. Our analysis revealed that naive (_N), central memory (_CM), and effector/memory (_Eff/Mem) CD32a⁺ CD4⁺ T-cell clusters that co-express LILRA2- and CD64-activating receptors were more abundant in primary HIV infection and cART stages. Conversely, LILRA2⁻ CD32a⁺ CD4⁺ T-cell clusters of either the T_N, T_CM, or T_Eff/Mem phenotype were more abundant in healthy individuals. Finally, an activated CD32a⁺ CD4⁺ T_Eff/Mem cell cluster co-expressing LILRA2, CD57, and NKG2C was more abundant in all HIV stages, particularly during primary HIV infection. Overall, our data show that multiple abundance modifications of CD32a⁺ CD4⁺ T-cell subsets occur in the early phase of HIV infection, and some of which are conserved after effective cART. Our study brings a better comprehension of the relationship between CD32a expression and CD4⁺ T cells during HIV infection.</p

image_9_Mass Cytometry Analysis Reveals the Landscape and Dynamics of CD32a+ CD4+ T Cells From Early HIV Infection to Effective cART.PDF

<p>CD32a has been proposed as a specific marker of latently HIV-infected CD4⁺ T cells. However, CD32a was recently found to be expressed on CD4⁺ T cells of healthy donors, leading to controversy on the relevance of this marker in HIV persistence. Here, we used mass cytometry to characterize the landscape and variation in the abundance of CD32a⁺ CD4⁺ T cells during HIV infection. To this end, we analyzed CD32a⁺ CD4⁺ T cells in primary HIV infection before and after effective combination antiretroviral therapy (cART) and in healthy donors. We found that CD32a⁺ CD4⁺ T cells include heterogeneous subsets that are differentially affected by HIV infection. Our analysis revealed that naive (_N), central memory (_CM), and effector/memory (_Eff/Mem) CD32a⁺ CD4⁺ T-cell clusters that co-express LILRA2- and CD64-activating receptors were more abundant in primary HIV infection and cART stages. Conversely, LILRA2⁻ CD32a⁺ CD4⁺ T-cell clusters of either the T_N, T_CM, or T_Eff/Mem phenotype were more abundant in healthy individuals. Finally, an activated CD32a⁺ CD4⁺ T_Eff/Mem cell cluster co-expressing LILRA2, CD57, and NKG2C was more abundant in all HIV stages, particularly during primary HIV infection. Overall, our data show that multiple abundance modifications of CD32a⁺ CD4⁺ T-cell subsets occur in the early phase of HIV infection, and some of which are conserved after effective cART. Our study brings a better comprehension of the relationship between CD32a expression and CD4⁺ T cells during HIV infection.</p

image_7_Mass Cytometry Analysis Reveals the Landscape and Dynamics of CD32a+ CD4+ T Cells From Early HIV Infection to Effective cART.PDF

<p>CD32a has been proposed as a specific marker of latently HIV-infected CD4⁺ T cells. However, CD32a was recently found to be expressed on CD4⁺ T cells of healthy donors, leading to controversy on the relevance of this marker in HIV persistence. Here, we used mass cytometry to characterize the landscape and variation in the abundance of CD32a⁺ CD4⁺ T cells during HIV infection. To this end, we analyzed CD32a⁺ CD4⁺ T cells in primary HIV infection before and after effective combination antiretroviral therapy (cART) and in healthy donors. We found that CD32a⁺ CD4⁺ T cells include heterogeneous subsets that are differentially affected by HIV infection. Our analysis revealed that naive (_N), central memory (_CM), and effector/memory (_Eff/Mem) CD32a⁺ CD4⁺ T-cell clusters that co-express LILRA2- and CD64-activating receptors were more abundant in primary HIV infection and cART stages. Conversely, LILRA2⁻ CD32a⁺ CD4⁺ T-cell clusters of either the T_N, T_CM, or T_Eff/Mem phenotype were more abundant in healthy individuals. Finally, an activated CD32a⁺ CD4⁺ T_Eff/Mem cell cluster co-expressing LILRA2, CD57, and NKG2C was more abundant in all HIV stages, particularly during primary HIV infection. Overall, our data show that multiple abundance modifications of CD32a⁺ CD4⁺ T-cell subsets occur in the early phase of HIV infection, and some of which are conserved after effective cART. Our study brings a better comprehension of the relationship between CD32a expression and CD4⁺ T cells during HIV infection.</p