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Titolo:
The coreceptor mutation CCR5 Delta 32 influences the dynamics of HIV epidemics and is selected for by HIV
Autore:
Sullivan, AD; Wigginton, J; Kirschner, D;
Indirizzi:
Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 l & Immunol, Ann Arbor, MI 48109 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 18, volume: 98, anno: 2001,
pagine: 10214 - 10219
SICI:
0027-8424(20010828)98:18<10214:TCMCD3>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-IMMUNODEFICIENCY-VIRUS; SEXUALLY-TRANSMITTED DISEASES; CHEMOKINE RECEPTOR GENE; DEVELOPING-COUNTRIES; HETEROSEXUAL TRANSMISSION; SENSITIVITY ANALYSIS; GLOBAL DISTRIBUTION; FUSION COFACTORS; COMPUTER-MODELS; VIRAL PHENOTYPE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
66
Recensione:
Indirizzi per estratti:
Indirizzo: Kirschner, D Univ Michigan, Sch Med, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 Ann Arbor, MI 48109 USA
Citazione:
A.D. Sullivan et al., "The coreceptor mutation CCR5 Delta 32 influences the dynamics of HIV epidemics and is selected for by HIV", P NAS US, 98(18), 2001, pp. 10214-10219

Abstract

We explore the impact of a host genetic factor on heterosexual HIV epidemics by using a deterministic mathematical model. A protective allele unequally distributed across populations is exemplified in our models by the 32-bpdeletion in the host-cell chemokine receptor CCR5, CCR5 Delta 32. Individuals homozygous for CCR5 Delta 32 are protected against HIV infection whereas those heterozygous for CCR5A32 have lower pre-AIDS viral loads and delayed progression to AIDS. CCR5A32 may limit HIV spread by decreasing the probability of both risk of infection and infectiousness. In this work, we characterize epidemic HIV within three dynamic subpopulations: CCR5/CCR5 (homozygous, wild type), CCR5/CCR5 Delta 32 (heterozygous), and CCR5 Delta 32/CCR5Delta 32 (homozygous, mutant). Our results indicate that prevalence of HIV/ AIDS is greater in populations lacking the CCR5A32 alleles (homozygous wild types only) as compared with populations that include people heterozygous or homozygous for CCR5 Delta 32. Also, we show that HIV can provide selective pressure for CCR5 Delta 32, increasing the frequency of this allele.

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Documento generato il 27/11/20 alle ore 15:20:06