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HIV Drug Therapy in the Americas 16-18 April 2015, Mexico City, Mexico.

- J Int AIDS Soc (2015)

View Article: PubMed Central - PubMed

ABSTRACT

Antiretroviral therapies have proved life-saving in HIV infection, dramatically reducing morbidity and mortality. With longer survival, morbidities and mortalities in HIV infection are increasingly similar to the morbidities and mortalities associated with ageing. In treated HIV infection, the risk of these morbidities and mortalities is linked to immune activation, inflammation and coagulation indices. And in persons with treated HIV infection, failure to restore circulating CD4 T cell numbers is associated with a greater risk of morbidities and mortalities as well as to heightened levels of inflammation and coagulation. The drivers of immune activation, inflammation and coagulation in treated HIV infection are incompletely defined and could be related to sustained low levels of viral replication in tissues, to translocation of microbial products across a damaged gut mucosa, to replication of co-pathogens such as cytomegalovirus, to increased levels of inflammatory lipids, or to homeostatic responses to lymphocytopenia that may drive expansion of CD8 T cell numbers. We present here models that link inflammation and coagulation to morbid outcomes as well as to the pathogenesis of CD4 T cell restoration failure and CD8 T cell expansion.

No MeSH data available.


Median time since all OIs and non-TB OIs.
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F0001_20109: Median time since all OIs and non-TB OIs.

Mentions: A total of 20,148 patients were included; 1558 patients had an OI before HAART initiation and were included in the analysis: 207 from Argentina, 746 from Brazil, 322 from Chile, 112 from Honduras and 171 from Mexico. The proportion of patients who started treatment within four weeks of the OI was statistically different between sites (p<0.001). Median time since all OIs and non-TB OIs to HAART initiation decreased from 41 (IQR: 20–85) days before 2009 to 30 (IQR: 14–50) after 2009 (Figure 1). Factors associated with Early HAART group were CD4+ at HAART initiation <200 cell/mm3 (p<0.001), non- tuberculosis OI (p<0.001), site and year of initiation (before 2009; p<0.001).


HIV Drug Therapy in the Americas 16-18 April 2015, Mexico City, Mexico.

- J Int AIDS Soc (2015)

Median time since all OIs and non-TB OIs.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4401943&req=5

F0001_20109: Median time since all OIs and non-TB OIs.
Mentions: A total of 20,148 patients were included; 1558 patients had an OI before HAART initiation and were included in the analysis: 207 from Argentina, 746 from Brazil, 322 from Chile, 112 from Honduras and 171 from Mexico. The proportion of patients who started treatment within four weeks of the OI was statistically different between sites (p<0.001). Median time since all OIs and non-TB OIs to HAART initiation decreased from 41 (IQR: 20–85) days before 2009 to 30 (IQR: 14–50) after 2009 (Figure 1). Factors associated with Early HAART group were CD4+ at HAART initiation <200 cell/mm3 (p<0.001), non- tuberculosis OI (p<0.001), site and year of initiation (before 2009; p<0.001).

View Article: PubMed Central - PubMed

ABSTRACT

Antiretroviral therapies have proved life-saving in HIV infection, dramatically reducing morbidity and mortality. With longer survival, morbidities and mortalities in HIV infection are increasingly similar to the morbidities and mortalities associated with ageing. In treated HIV infection, the risk of these morbidities and mortalities is linked to immune activation, inflammation and coagulation indices. And in persons with treated HIV infection, failure to restore circulating CD4 T cell numbers is associated with a greater risk of morbidities and mortalities as well as to heightened levels of inflammation and coagulation. The drivers of immune activation, inflammation and coagulation in treated HIV infection are incompletely defined and could be related to sustained low levels of viral replication in tissues, to translocation of microbial products across a damaged gut mucosa, to replication of co-pathogens such as cytomegalovirus, to increased levels of inflammatory lipids, or to homeostatic responses to lymphocytopenia that may drive expansion of CD8 T cell numbers. We present here models that link inflammation and coagulation to morbid outcomes as well as to the pathogenesis of CD4 T cell restoration failure and CD8 T cell expansion.

No MeSH data available.