Profound differences in virus population genetics correspond to protection from CD4 decline resulting from feline lentivirus coinfection.
Profound differences in virus population genetics correspond to protection from CD4 decline resulting from feline lentivirus coinfection.
复制标题
DOI：
10.3390/v2122663
复制
发表时间：
2010-12
期刊：
影响因子：
--
通讯作者：
Poss M
中科院分区：
文献类型：
--
作者：
Padhi A;Ross H;Terwee J;Vandewoude S;Poss M
CD4 下降是感染猫免疫缺陷病毒 (FIV) 或人类免疫缺陷病毒 1 型 (HIV-1) 的个体发病的标志。在接触强毒 FIV 毒株 (FIVC) 之前感染复制性差的非致病性 FIV (PLV) 的猫通过与可测量的适应性免疫反应或循环病毒载量减少无关的机制维持 CD4 数量。我们采用基于病毒基因组 3' 部分的群体遗传学方法来估计单次和双重感染猫的 FIVC 群体结构。在双重感染的猫中，FIVC有效种群规模在最初的病毒扩张阶段下降，感染三周后，种群数量急剧下降。 FIVC 群体在 FIVC 感染后大约七周恢复到瓶颈前水平。然而，根据对时间种群结构和替代概况的估计，从双重感染猫的瓶颈中出现的种群是不同的。在双重感染的猫中，从早期到晚期，转换率比率（κ）的转变主要是由于转换的减少，而在单次感染的猫中，κ随着时间的推移而下降。尽管在瓶颈期间从双重感染的猫中回收了一个具有广泛的 G 到 A 替换（表明宿主胞苷脱氨酶编辑）的克隆，但瓶颈后群体的 G 到 A 替换总体减少。这些数据与 PLV 诱导的宿主限制模型一致，推测涉及宿主 DNA 编辑，该模型改变了整个感染过程中 FIVC 的动态，导致疾病减弱。
CD4 decline is a hallmark of disease onset in individuals infected with Feline Immunodeficiency Virus (FIV) or Human Immunodeficiency Virus type 1 (HIV-1). Cats that are infected with a poorly replicating, apathogenic FIV (PLV) prior to exposure to a virulent FIV strain (FIVC) maintain CD4 numbers by mechanisms that are not correlated with a measurable adaptive immune response or reduction in circulating viral load. We employed population genetic approaches based on the 3′ portion of the viral genome to estimate the population structure of FIVC from single and dual infected cats. In dual infected cats, FIVC effective population size was decreased during the initial viral expansion phase, and after three weeks of infection, the population declined sharply. The FIVC population recovered to pre-bottleneck levels approximately seven weeks post-FIVC infection. However, the population emerging from the bottleneck in dual infected cats was distinct based on estimates of temporal population structure and substitution profiles. The transition to transversion rate ratio (κ) increased from early to late phases in dual infected cats due primarily to a decrease in transversions whereas in single infected cats, κ declined over time. Although one clone with extensive G to A substitutions, indicative of host cytidine deaminase editing, was recovered from a dual infected cat during the bottleneck, the post bottleneck population had an overall reduction in G to A substitutions. These data are consistent with a model of PLV-induced host restriction, putatively involving host DNA editing, that alters the dynamics of FIVC throughout the course of infection leading to disease attenuation.
登录
查看更多内容
影响因子：
3.7
作者：
Becquart, P;Chomont, N;Hocini, H
通讯作者：
Hocini, H
影响因子：
64.5
作者：
Harris, RS;Bishop, KN;Malim, MH
通讯作者：
Malim, MH
影响因子：
5.4
作者：
Koning, Fransje A.;Newman, Edmund N. C.;Malim, Michael H.
通讯作者：
Malim, Michael H.
影响因子：
5.4
作者：
CLARKE, DK;DUARTE, EA;HOLLAND, J
通讯作者：
HOLLAND, J
影响因子：
2.7
作者：
Hayward, Jessica J.;Rodrigo, Allen G.
通讯作者：
Rodrigo, Allen G.