Viral loads in dual infection with HIV-1 and cytomegalovirus

Boriskin, Yu. S.; Sharland, Mike; Dalton, Ruth; duMont, Gill; Booth, James C.

doi:10.1136/adc.80.2.132

Cited by 6 publications

(5 citation statements)

References 32 publications

(24 reference statements)

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“…Furthermore, of great importance with respect to HIV-1 transmission is the finding that HIV-1 can frequently be detected in genital ulcers caused by HSV-2 in men (299). The levels of CMV and HIV-1 in plasma appear to be independent of one another (35), and the CMV load and HIV-1 proviral load in autopsy tissues were found to be discordant (94). Although shedding of HIV-1 in semen is positively associated with shedding of CMV, the two processes appear to have independent immunological controls (181).…”

Section: Viral Infectionsmentioning

confidence: 99%

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

Lawn

Butera²,

Folks³

2001

Clin Microbiol Rev

254

216

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The life cycle of human immunodeficiency virus type 1 (HIV-1) is intricately related to the activation state of the host cells supporting viral replication. Although cellular activation is essential to mount an effective host immune response to invading pathogens, paradoxically the marked systemic immune activation that accompanies HIV-1 infection in vivo may play an important role in sustaining phenomenal rates of HIV-1 replication in infected persons. Moreover, by inducing CD4+ cell loss by apoptosis, immune activation may further be central to the increased rate of CD4+ cell turnover and eventual development of CD4+ lymphocytopenia. In addition to HIV-1-induced immune activation, exogenous immune stimuli such as opportunistic infections may further impact the rate of HIV-1 replication systemically or at localized anatomical sites. Such stimuli may also lead to genotypic and phenotypic changes in the virus pool. Together, these various immunological effects on the biology of HIV-1 may potentially enhance disease progression in HIV-infected persons and may ultimately outweigh the beneficial aspects of antiviral immune responses. This may be particularly important for those living in developing countries, where there is little or no access to antiretroviral drugs and where frequent exposure to pathogenic organisms sustains a chronically heightened state of immune activation. Moreover, immune activation associated with sexually transmitted diseases, chorioamnionitis, and mastitis may have important local effects on HIV-1 replication that may increase the risk of sexual or mother-to-child transmission of HIV-1. The aim of this paper is to provide a broad review of the interrelationship between immune activation and the immunopathogenesis, transmission, progression, and treatment of HIV-1 infection in vivo

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Section: Viral Infectionsmentioning

confidence: 99%

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

Lawn

Butera²,

Folks³

2001

Clin Microbiol Rev

254

216

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“…In order to understand the mechanisms that underlie the relationship between CMV coinfection and rapid HIV-1 disease progression, it is first necessary to determine the incidence of CMV infection among HIV-infected infants and to describe its natural history. Although risk factors associated with vertical CMV transmission are well defined, very few studies [22,23] have measured CMV replication quantitatively in infants, and only one longitudinal study [24] has described infant CMV viral load in the setting of HIV-1. The purpose of our study was to describe the incidence and timing of CMV infection and the kinetics of CMV viral replication in HIV-infected and HIV-exposed uninfected Kenyan infants.…”

Section: Introductionmentioning

confidence: 99%

Acute cytomegalovirus infection in Kenyan HIV-infected infants

Slyker

Lohman-Payne

John‐Stewart

et al. 2009

Aids

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Objective Cytomegalovirus (CMV) coinfection may influence HIV-1 disease progression during infancy. Our aim was to describe the incidence of CMV infection and the kinetics of viral replication in Kenyan HIV-infected and HIV-exposed uninfected infants. Methods HIV-1 and CMV plasma viral loads were serially measured in 20 HIV-exposed uninfected and 44 HIV-infected infants born to HIV-infected mothers. HIV-infected children were studied for the first 2 years of life, and HIV-exposed uninfected infants were studied for 1 year. Results CMV DNA was detected frequently during the first months of life; by 3 months of age, CMV DNA was detected in 90% of HIV-exposed uninfected infants and 93% of infants who had acquired HIV-1 in utero. CMV viral loads were highest in the 1–3 months following the first detection of virus and declined rapidly thereafter. CMV peak viral loads were significantly higher in the HIV-infected infants compared with the HIV-exposed uninfected infants (mean 3.2 versus 2.7 log10 CMV DNA copies/ml, respectively, P = 0.03). The detection of CMV DNA persisted to 7–9 months post-CMV infection in both the HIV-exposed uninfected (8/17, 47%) and HIV-infected (13/18, 72%, P = 0.2) children. Among HIV-infected children, CMV DNA was detected in three of the seven (43%) surviving infants tested between 19 and 21 months post-CMV infection. Finally, a strong correlation was found between peak CMV and HIV-1 viral loads (ρ = 0.40, P = 0.008). Conclusion Acute CMV coinfection is common in HIV-infected Kenyan infants. HIV-1 infection was associated with impaired containment of CMV replication.

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“…The significantly higher CMV viral load in the youngest age group (0–2 years) could explain the generally higher mortality in this age group due to the accelerated disease progression 2. However, the conclusion regarding the progression of HIV infection associated with the CMV viral load in this cross sectional study1 should be treated with caution.…”

mentioning

confidence: 72%

“…E ditor ,—The paper by Boriskin and colleagues1 provides interesting information regarding the age related contribution of cytomegalovirus (CMV) viral load in HIV infected children. The significantly higher CMV viral load in the youngest age group (0–2 years) could explain the generally higher mortality in this age group due to the accelerated disease progression 2.…”

mentioning

confidence: 99%