Determination of simian immunodeficiency virus production by infected activated and resting cells

• Published in: AIDS (London) Vol. 21; no. 2; pp. 163 - 168
• Main Authors: REILLY, Cavan, WIETGREFE, Steve, SEDGEWICK, Gerald, HAASE, Ashley
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 11.01.2007
• Subjects: AIDS/HIV; Animals; Biological and medical sciences; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - virology; Human viral diseases; Infectious diseases; Lymphocyte Activation; Macaca mulatta; Medical sciences; Models, Biological; Simian Acquired Immunodeficiency Syndrome - immunology; Simian Acquired Immunodeficiency Syndrome - virology; Simian immunodeficiency virus; Simian Immunodeficiency Virus - physiology; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Virion - physiology; Virus Replication; Virus; Infection; HIV-1; Virion; virion production; Retroviridae; Infected cell; Simian immunodeficiency virus; Lentivirus
• ISSN: 0269-9370; 1473-5571
• DOI: 10.1097/QAD.0b013e328012565b

To determine the relative amount of virus produced by activated and resting CD4+ T cells. The total quantity of virus produced by an activated cell relative to a resting cell in vivo was estimated from 'snap-shots' of virus production by infected cells at one time point. Bayesian statistical methods were used to determine a credible interval for the desired ratio. The posterior mean of the ratio of virus produced by a typical activated cell to a typical resting cell is 0.82 to 4.28, depending on the half-lives of the resting infected cells. Simian immunodeficiency virus-infected resting cells could accordingly be responsible for 70 to 93% of peak virus production in the acute stage of infection. Whereas in 'snap-shots' the infected resting cells apparently produce much less virus than infected activated CD4+ T cells, the coincidence of peak SIV production with predominant infection of resting cells along with longer half-lives for productively infected resting cells point to a major contribution to virus production in early infection.