Hyperthermia stimulates HIV-1 replication.
HIV-infected individuals may experience fever episodes. Fever is an elevation of the body temperature accompanied by inflammation. It is usually beneficial for the host through enhancement of immunological defenses. In cultures, transient non-physiological heat shock (42-45°C) and Heat Shock Protein...
Saved in:
| Main Authors: | , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2012-01-01
|
| Series: | PLoS Pathogens |
| Online Access: | https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1002792&type=printable |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1849434121295626240 |
|---|---|
| author | Ferdinand Roesch Oussama Meziane Anna Kula Sébastien Nisole Françoise Porrot Ian Anderson Fabrizio Mammano Ariberto Fassati Alessandro Marcello Monsef Benkirane Olivier Schwartz |
| author_facet | Ferdinand Roesch Oussama Meziane Anna Kula Sébastien Nisole Françoise Porrot Ian Anderson Fabrizio Mammano Ariberto Fassati Alessandro Marcello Monsef Benkirane Olivier Schwartz |
| author_sort | Ferdinand Roesch |
| collection | DOAJ |
| description | HIV-infected individuals may experience fever episodes. Fever is an elevation of the body temperature accompanied by inflammation. It is usually beneficial for the host through enhancement of immunological defenses. In cultures, transient non-physiological heat shock (42-45°C) and Heat Shock Proteins (HSPs) modulate HIV-1 replication, through poorly defined mechanisms. The effect of physiological hyperthermia (38-40°C) on HIV-1 infection has not been extensively investigated. Here, we show that culturing primary CD4+ T lymphocytes and cell lines at a fever-like temperature (39.5°C) increased the efficiency of HIV-1 replication by 2 to 7 fold. Hyperthermia did not facilitate viral entry nor reverse transcription, but increased Tat transactivation of the LTR viral promoter. Hyperthermia also boosted HIV-1 reactivation in a model of latently-infected cells. By imaging HIV-1 transcription, we further show that Hsp90 co-localized with actively transcribing provirus, and this phenomenon was enhanced at 39.5°C. The Hsp90 inhibitor 17-AAG abrogated the increase of HIV-1 replication in hyperthermic cells. Altogether, our results indicate that fever may directly stimulate HIV-1 replication, in a process involving Hsp90 and facilitation of Tat-mediated LTR activity. |
| format | Article |
| id | doaj-art-2904f06c52d8441fa5fddd36e9607a8d |
| institution | Kabale University |
| issn | 1553-7366 1553-7374 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Pathogens |
| spelling | doaj-art-2904f06c52d8441fa5fddd36e9607a8d2025-08-20T03:26:47ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742012-01-0187e100279210.1371/journal.ppat.1002792Hyperthermia stimulates HIV-1 replication.Ferdinand RoeschOussama MezianeAnna KulaSébastien NisoleFrançoise PorrotIan AndersonFabrizio MammanoAriberto FassatiAlessandro MarcelloMonsef BenkiraneOlivier SchwartzHIV-infected individuals may experience fever episodes. Fever is an elevation of the body temperature accompanied by inflammation. It is usually beneficial for the host through enhancement of immunological defenses. In cultures, transient non-physiological heat shock (42-45°C) and Heat Shock Proteins (HSPs) modulate HIV-1 replication, through poorly defined mechanisms. The effect of physiological hyperthermia (38-40°C) on HIV-1 infection has not been extensively investigated. Here, we show that culturing primary CD4+ T lymphocytes and cell lines at a fever-like temperature (39.5°C) increased the efficiency of HIV-1 replication by 2 to 7 fold. Hyperthermia did not facilitate viral entry nor reverse transcription, but increased Tat transactivation of the LTR viral promoter. Hyperthermia also boosted HIV-1 reactivation in a model of latently-infected cells. By imaging HIV-1 transcription, we further show that Hsp90 co-localized with actively transcribing provirus, and this phenomenon was enhanced at 39.5°C. The Hsp90 inhibitor 17-AAG abrogated the increase of HIV-1 replication in hyperthermic cells. Altogether, our results indicate that fever may directly stimulate HIV-1 replication, in a process involving Hsp90 and facilitation of Tat-mediated LTR activity.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1002792&type=printable |
| spellingShingle | Ferdinand Roesch Oussama Meziane Anna Kula Sébastien Nisole Françoise Porrot Ian Anderson Fabrizio Mammano Ariberto Fassati Alessandro Marcello Monsef Benkirane Olivier Schwartz Hyperthermia stimulates HIV-1 replication. PLoS Pathogens |
| title | Hyperthermia stimulates HIV-1 replication. |
| title_full | Hyperthermia stimulates HIV-1 replication. |
| title_fullStr | Hyperthermia stimulates HIV-1 replication. |
| title_full_unstemmed | Hyperthermia stimulates HIV-1 replication. |
| title_short | Hyperthermia stimulates HIV-1 replication. |
| title_sort | hyperthermia stimulates hiv 1 replication |
| url | https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1002792&type=printable |
| work_keys_str_mv | AT ferdinandroesch hyperthermiastimulateshiv1replication AT oussamameziane hyperthermiastimulateshiv1replication AT annakula hyperthermiastimulateshiv1replication AT sebastiennisole hyperthermiastimulateshiv1replication AT francoiseporrot hyperthermiastimulateshiv1replication AT iananderson hyperthermiastimulateshiv1replication AT fabriziomammano hyperthermiastimulateshiv1replication AT aribertofassati hyperthermiastimulateshiv1replication AT alessandromarcello hyperthermiastimulateshiv1replication AT monsefbenkirane hyperthermiastimulateshiv1replication AT olivierschwartz hyperthermiastimulateshiv1replication |