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1.
Figure 2

Figure 2. V1V2 length vs. time since infection (upper panel) and vs. year of sampling (lower panel).. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

Lengths are indicated in amino acids. Overlapping data points appear as darker symbols. Sequences from plasma are represented by diamonds and sequences from PBMC are represented by circles. Regression coefficients and coefficients of determination are shown for univariate linear regression, for plasma (red line) and PBMC (blue line).

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.
2.
Figure 5

Figure 5. V1V2 length vs. time in subjects Q23, CC1 and 1362.. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

Panel A: Subject Q23, infected with HIV subtype A. Sequences were derived from PBMC (black circles), plasma (black diamonds) and DNA from cervical lymphocytes (green squares) as described by Poss et al [80]. Panel B: Subject CC1, infected with subtype A. Sequences were obtained from plasma (black diamonds) and tissue culture (red squares). Length change of in vitro sequences occurs over ∼ 40 days, and are represented along an expanded X-axis for clarity.

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.
3.
Figure 6

Figure 6. V1V2 loop lengths over time in group L2.. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

Sequences from plasma are represented by diamonds and sequences from PBMC are represented by circles. Significant slopes are indicated in bold. X-axis denotes years elapsed between sampling time points, but do not necessarily indicate the total duration of infection. The first author of the report in which data were originally presented are indicated in the upper left-hand corner of each graph. Group L2 subjects were reported to have an AIDS-defining illness or peripheral CD4 count <200/mm3 between the first and second samples.

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.
4.
Figure 3

Figure 3. Correlation between stage of illness and V1V2 length.. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

Lengths are indicated in amino acids. Sequences from plasma are represented by diamonds and sequences from PBMC are represented by circles. Overlapping data points appear as darker symbols. Quartiles and median values are indicated by horizontal line segments. Stage 1, 2, and 3 subjects were sampled within two months, between two months and three years, and at times >3 years post infection, respectively. Stage 4 subjects were comprised of all individuals meeting 1993 CDC criteria for AIDS when sampling occurred, regardless of time since infection.

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.
5.
Figure 4

Figure 4. V1V2 loop lengths over time in group L1.. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

Sequences from plasma are represented by diamonds and sequences from PBMC are represented by circles. Significant slopes are indicated in bold. X-axis denotes years elapsed between sampling time points, but do not necessarily indicate the total duration of infection. The first author of the report in which data were originally presented is indicated in the upper left-hand corner of each graph. Group L1 subjects did not meet criteria for AIDS at any time prior to the final sample. Subjects reported by McDonald et al had received AZT monotherapy at one or more times prior to sampling.

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.
6.
Figure 7

Figure 7. Proposed evolution of V1V2 loop size change during transmission and HIV infection.. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

At the time of sexual transmission, a significant genetic bottleneck occurs in which one or a small number of donor variants is transmitted to the recipient, without clear selection for loop size (represented on the y-axis). During early infection, prior to an effective host response, viral variants with a compact V1V2 loop have a competitive advantage, and V1V2 loop size remains stable or regresses. During chronic asymptomatic infection, mean V1V2 length increases in response to (humoral) immune selective pressure. As immune function wanes, V1V2 loop length gradually declines.

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.
7.
Figure 1

Figure 1. Schematic diagram of HIV-1 env subregions (center bar) and distribution of subregion loop lengths (surrounding bar graphs).. From: HIV-1 Envelope Subregion Length Variation during Disease Progression.

The center bar depicts the linear arrangement of subregions V1V2 through V5 within the HIV Env gp120 protein. The amino acid length distribution of each subregion is shown in the linked bar graphs, including sequences in the cross-sectional dataset, the longitudinal dataset and the transmission data described in Text S1. Length distributions in V1V2 and V4 data are shown by isolation site (PBMC  =  blue bars, plasma  =  red bars, cervical cells  =  green bars, CSF  =  light gray bars, dendritic cells  =  orange bars, cell culture  =  dark gray bars, and cells from unknown anatomic compartments represented by open bars), and by subtype (subtype B  =  blue bars, subtype A  =  red bars, subtype C  =  green bars, subtype G  =  orange bars, untyped sequences  =  open bars). V5 sequences were all of subtype B. X-axis: sequence length (amino acids); Y-axis: number of sequences.

Marcel E. Curlin, et al. PLoS Pathog. 2010 December;6(12):e1001228.

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