Cross-sectional detection of acute HIV infection: timing of transmission, inflammation and antiretroviral therapy.
Oliver Dibben,Jeffrey A. Anderson,Andrea Stacey,Ashley J Mayo,Philip J. Norris,Philip J. Norris,Jo Ann D. Kuruc,Jesus F. Salazar-Gonzalez,Hui Li,Brandon F. Keele,Charles B. Hicks,David M. Margolis,Guido Ferrari,Barton F. Haynes,Ronald Swanstrom,George M. Shaw,Beatrice H. Hahn,Joseph J. Eron,Persephone Borrow,Myron S. Cohen +19 more
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TLDR
Improved AHI detection is urgently needed given the difficulty in recruiting subjects early in AHI, and viral sequence diversity proved accurate in estimating time of infection.Abstract:
Background: Acute HIV infection (AHI) is a critical phase of infection when irreparable damage to the immune system occurs and subjects are very infectious. We studied subjects with AHI prospectively to develop better treatment and public health interventions. Methods: Cross-sectional screening was employed to detect HIV RNA positive, antibody negative subjects. Date of HIV acquisition was estimated from clinical history and correlated with sequence diversity assessed by single genome amplification (SGA). Twenty-two cytokines/chemokines were measured from enrollment through week 24. Results: Thirty-seven AHI subjects were studied. In 7 participants with limited exposure windows, the median exposure to HIV occurred 14 days before symptom onset. Lack of viral sequence diversification confirmed the short duration of infection. Transmission dates estimated by SGA/sequencing using molecular clock models correlated with transmission dates estimated by symptom onset in individuals infected with single HIV variants (mean of 28 versus 33 days). Only 10 of 22 cytokines/chemokines were significantly elevated among AHI participants at enrollment compared to uninfected controls, and only 4 participants remained seronegative at enrollment.read more
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Prospective Study of Acute HIV-1 Infection in Adults in East Africa and Thailand
Merlin L. Robb,Leigh Anne Eller,Hannah Kibuuka,Kathleen Rono,Lucas Maganga,Sorachai Nitayaphan,Eugene Kroon,Fred Sawe,Samuel Sinei,Somchai Sriplienchan,Linda L. Jagodzinski,Jennifer A. Malia,Mark M. Manak,Mark de Souza,Sodsai Tovanabutra,Eric Sanders-Buell,Morgane Rolland,Julie Dorsey-Spitz,Michael A. Eller,Mark Milazzo,Qun Li,Andrew Lewandowski,Hao Wu,Edith Swann,Robert J. O'Connell,Sheila A. Peel,Peter Dawson,Jerome H. Kim,Nelson L. Michael +28 more
TL;DR: Few symptoms and signs were observed during acute HIV-1 infection, and they were most common before peak viremia, which was nearly equivalent to the viral-load set point.
Journal ArticleDOI
Immediate antiviral therapy appears to restrict resting CD4+ cell HIV-1 infection without accelerating the decay of latent infection.
Nancie M. Archin,Naveen K. Vaidya,Naveen K. Vaidya,Jo Ann D. Kuruc,Abigail L. Liberty,Ann Wiegand,Mary F. Kearney,Myron S. Cohen,John M. Coffin,Ronald J. Bosch,Joseph J. Eron,David M. Margolis,Alan S. Perelson +12 more
TL;DR: In the largest cohort of patients treated during acute seronegative HIV infection (AHI) in whom RCI has been stringently quantified, it is found that early ART reduced the generation of latently infected cells, reinforcing and extending the concept that new approaches will be needed to eradicate HIV infection.
Journal ArticleDOI
Fitness Costs and Diversity of the Cytotoxic T Lymphocyte (CTL) Response Determine the Rate of CTL Escape during Acute and Chronic Phases of HIV Infection
Vitaly V. Ganusov,N Goonetilleke,Michael K. P. Liu,Guido Ferrari,George M. Shaw,Andrew J. McMichael,Persephone Borrow,Bette T. Korber,Bette T. Korber,Alan S. Perelson +9 more
TL;DR: It is found that the rate of viral escape from CTL responses in a given patient decreases dramatically from acute infection to the viral set point at 1 year after the infection.
Journal ArticleDOI
Acute Plasma Biomarkers of T Cell Activation Set-Point Levels and of Disease Progression in HIV-1 Infection
Anne-Sophie Liovat,Anne-Sophie Liovat,Marie-Anne Rey-Cuille,Camille Lécuroux,Beatrice Jacquelin,Isabelle Girault,Gaël Petitjean,Yasmine Zitoun,Alain Venet,Françoise Barré-Sinoussi,Pierre Lebon,Laurence Meyer,Martine Sinet,Michaela Müller-Trutwin +13 more
TL;DR: This study shows that the inflammatory profile in primary HIV-1 infection is associated with T cell activation levels and CD4+ T cell counts at set-point, and plasma IP-10 levels were of strong predictive value for rapid disease progression.
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Insights into B cells and HIV-specific B-cell responses in HIV-infected individuals.
Susan Moir,Anthony S. Fauci +1 more
TL;DR: B‐cell perturbations in HIV‐infected individuals are discussed, focusing on the skewing of B‐cell subsets that circulate in the peripheral blood and their counterparts that reside in lymphoid tissues.
References
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Richard A. Koup,Jeffrey T. Safrit,Yunzhen Cao,C. A. Andrews,G. Mcleod,William Borkowsky,C. Farthing,David D. Ho +7 more
TL;DR: It is suggested that cellular immunity is involved in the initial control of virus replication in primary HIV-1 infection and a role for CTL in protective immunity to HIV- 1 in vivo is indicated.
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Journal ArticleDOI
Identification and characterization of transmitted and early founder virus envelopes in primary HIV-1 infection
Brandon F. Keele,Elena E. Giorgi,Elena E. Giorgi,Jesus F. Salazar-Gonzalez,Julie M. Decker,Kimmy T. Pham,Maria G. Salazar,Chuanxi Sun,Truman Grayson,Shuyi Wang,Hui Li,Xiping Wei,Chunlai Jiang,Jennifer L. Kirchherr,Feng Gao,Jeffery A. Anderson,Li Hua Ping,Ronald Swanstrom,Georgia D. Tomaras,William A. Blattner,Paul A. Goepfert,J. Michael Kilby,Michael S. Saag,Eric Delwart,Michael P. Busch,Myron S. Cohen,David C. Montefiori,Barton F. Haynes,Brian Gaschen,Gayathri Athreya,Ha Y. Lee,Natasha T. Wood,Cathal Seoighe,Alan S. Perelson,Tanmoy Bhattacharya,Tanmoy Bhattacharya,Bette T. Korber,Bette T. Korber,Beatrice H. Hahn,George M. Shaw +39 more
TL;DR: A mathematical model of random viral evolution and phylogenetic tree construction is developed and used to analyze 3,449 complete env sequences derived by single genome amplification from 102 subjects with acute HIV-1 (clade B) infection, suggesting a finite window of potential vulnerability of HIV- 1 to vaccine-elicited immune responses, although phenotypic properties of transmitted Envs pose a formidable defense.
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