Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1997-3-26
pubmed:abstractText
BACKGROUND: Elucidation of the underlying rapid turnover of virus and HIV infected cells in vivo was perhaps the most informative and exciting discovery in HIV and AIDS research in the last few years. This observation, based on the rapid drop in virus load following antiviral drug therapy promises to change significantly the way we view important aspects of interaction of the virus and its host. As a result, the paradigm for HIV infection has shifted from considering the long period of clinical latency as one of viral inactivity, to viewing it as an active steady state of constant virus replication and cell death. This period should also be viewed as an integral part of the disease process, not simply a prolog to frank AIDS. METHODS: Here, I discuss the theoretical basis of the steady state model of HIV infection as well as its important consequences for understanding and controlling HIV pathogenesis. These include the significance of genetic variation and the establishment and evolution of the virus quasispecies, the evolution of resistance of the virus to antiviral therapy, and the theoretical and practical significance of virus load measurements. Emphasis is on discussion of recent developments as well as areas where our understanding still has significant gaps.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0269-9370
pubmed:author
pubmed:issnType
Print
pubmed:volume
10 Suppl 3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
S75-84
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
HIV viral dynamics.
pubmed:affiliation
Department of Molecular Biology and Microbiology, Tufts University, Boston, MA 02111, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't