Loss of cytomegalovirus (CMV) viraemia following highly active antiretroviral therapy in the absence of specific anti-CMV therapy

Deayton, Jane R; Mocroft, Amanda; Wilson, P; Emery, Vincent C.; Johnson, Margaret; Griffiths, Paul

doi:10.1097/00002030-199907090-00008

Cited by 96 publications

(48 citation statements)

References 15 publications

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“…The incidence of life-threatening complications has decreased dramatically with suppressive combination ART, likely due to restoration of CMV-specific immune responses that limit CMV reactivation [68]. While the clinical importance of CMV in the setting of ART-treated HIV disease is less clear, emerging evidence links CMV to suboptimal immune response to ART [61] and increased risk of non-AIDS-related complications [69].…”

Section: CMV Hiv and Clinical Outcomesmentioning

confidence: 99%

Cytomegalovirus and HIV: A Dangerous Pas de Deux

2016

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Human immunodeficiency virus (HIV)-infected adults who take stable antiretroviral therapy (ART) are at risk for early onset of agerelated diseases. This is likely due to a complex interaction between traditional risk factors, HIV infection itself, and other factors, such as underlying immune dysfunction and persistent inflammation. HIV disrupts the balance between the host and coinfecting microbes, worsening control of these potential pathogens. For example, HIV-infected adults are more likely than the general population to have subclinical bursts of cytomegalovirus (CMV) replication at mucosal sites. Production of antigens can activate the immune system and stimulate HIV replication, and it could contribute to the pathogenesis of adverse outcomes of aging, like cardiovascular disease and neurocognitive impairment. Further investigation of the relationships between CMV, immune dysfunction, and unsuccessful aging during chronic HIV infection is warranted.

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Section: CMV Hiv and Clinical Outcomesmentioning

confidence: 99%

Cytomegalovirus and HIV: A Dangerous Pas de Deux

2016

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“…According to Pomarico et al (2009), the protease inhibitors might have had an anti-candidiasis effect, resulting not only from immune reconstitution, but also from direct anti-yeast mechanisms. (Table II) Antiretroviral therapy benefits patients who are co-infected by HIV, HHV-8 (Harrington et al, 1997;Hocqueloux et al, 2001;Lebbe et al, 1998;Wit, Sol, Renwick, 1998), EBV (Hocqueloux et al, 2001), HBV (Benhamou et al, 2001;Deal et al, 2002;Perillo et al, 2000), parvovirus B19 (Mylonakis et al, 1999;Ware, Moore, 2001) and CMV (Borges et al, 2001;Deayton et al, 1999;Li et al, 1999).…”

Section: Antiretroviral Drugs and Fungal Agentsmentioning

confidence: 99%

Activity of antiretroviral drugs in human infections by opportunistic agents

Demarchi

Cardozo

Aristides

et al. 2012

Braz. J. Pharm. Sci.

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Highly active antiretroviral therapy (HAART) is used in patients infected with HIV. This treatment has been shown to significantly decrease opportunist infections such as those caused by viruses, fungi and particularly, protozoa. The use of HAART in HIV-positive persons is associated with immune reconstitution as well as decreased prevalence of oral candidiasis and candidal carriage. Antiretroviral therapy benefits patients who are co-infected by the human immunodeficiency virus (HIV), human herpes virus 8 (HHV-8), Epstein-Barr virus, hepatitis B virus (HBV), parvovirus B19 and cytomegalovirus (CMV). HAART has also led to a significant reduction in the incidence, and the modification of characteristics, of bacteremia by etiological agents such as Staphylococcus aureus, coagulase negative staphylococcus, non-typhoid species of Salmonella, Streptococcus pneumoniae, Pseudomonas aeruginosa, and Mycobacterium tuberculosis. HAART can modify the natural history of cryptosporidiosis and microsporidiosis, and restore mucosal immunity, leading to the eradication of Cryptosporidium parvum. A similar restoration of immune response occurs in infections by Toxoplasma gondii. The decline in the incidence of visceral leishmaniasis/HIV co-infection can be observed after the introduction of protease inhibitor therapy. Current findings are highly relevant for clinical medicine and may serve to reduce the number of prescribed drugs thereby improving the quality of life of patients with opportunistic diseases.
A terapia HAART (terapia antirretroviral altamente ativa) é usada em pacientes infectados pelo vírus da imunodeficiência humana (HIV) e demonstrou diminuição significativa de infecções oportunistas, tais como as causadas por vírus, fungos, protozoários e bactérias. O uso da HAART está associado com a reconstituição imunológica e diminuição na prevalência de candidíase oral. A terapia antirretroviral beneficia pacientes co-infectados pelo HIV, vírus herpes humano 8 (HHV-8), vírus Epstein-Barr (EBV), vírus da hepatite B (HBV), parvovírus B19 e citomegalovírus (CMV). A HAART também apresentou redução significativa da incidência e modificou as características da bacteremia por agentes etiológicos, tais como Staphylococcus aureus, espécies não-tifóides de Salmonella, Streptococcus pneumoniae, Pseudomonas aeruginosa, Mycobacterium tuberculosis. A HAART é capaz de modificar significativamente a história natural da criptosporidiose e microsporidiose. HAART pode efetivamente restaurar a imunidade da mucosa, levando à erradicação de Cryptosporidium parvum. Semelhante restauração da resposta imune ocorre em infecções por Toxoplasma gondii. O declínio na incidência de co-infecção leishmaniose visceral/HIV pode ser observada após a introdução da terapia com inibidores da protease. Os resultados atuais são altamente relevantes para a medicina clínica e podem proporcionar diminuição no número de prescrições medicamentosas e, consequentemente, melhor qualidade de vida para pacientes com doenças oportunistas

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“…To date, most studies addressing the effect of HAART on HCMV-specific immunity have been conducted in HIV patients in late stage disease either at high risk of developing HCMV or already presenting the latter. In these patients, control of HCMV replication, which rapidly follows response to HAART [Deayton et al, 1999], has been linked to recovery of lymphoproliferative response (LPR) to HCMV [Li et al, 1998;Gerna et al, 2001;Hsieh et al, 2001;Jacobson et al, 2001]; however, a number of studies have provided data showing that a lack of progression to HCMV disease is not always associated with the presence of robust LPRs to HCMV [Villacres et al, 2001;Weinberg et al, 2001;Berenguer et al, 2002;Tamarit et al, 2004]-thus seriously questioning the value of the LPRs to HCMV as a surrogate marker for protection against HCMV disease. Likewise, when evaluation of CD4 þ T cell immunity against HCMV in these patients has been assessed by flow cytometric detection of intracellular cytokines following short-term antigenic stimulation of PBMCs, an invariable association between the presence of HCMV disease and negative cytokine responses has not been proven [Jacobson et al, 2001].…”

Section: Introductionmentioning

confidence: 99%

Assessment of human cytomegalovirus specific T cell immunity in human immunodeficiency virus infected patients in different disease stages following HAART and in long‐term non‐progressors

Tamarit

Alberola

Mira

et al. 2004

Journal of Medical Virology

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T cell immunity to human cytomegalovirus (HCMV) was assessed in HAART-treated HIV-1 infected patients (9 asymptomatic, CDC group A; and 22 symptomatic, CDC group B), and in eight HIV-1 long term non-progressors. Patients were either prospectively or cross-sectionally examined for CD4(+) T cell counts, HIV RNA load, HCMV leukoDNAemia, HCMV DNA in urine, lymphoproliferative response (LPR) to HCMV and phytohemagglutinin (PHA), and cytokine secretion (IFN-gamma and IL-4) by HCMV-stimulated peripheral blood mononuclear cell (PBMC) cultures. No patient either progressed to clinical AIDS or developed HCMV active infection during the study period. Twenty-nine patients responded to HAART, though 12 patients failed to recover the LPR to HCMV over the study period (three from CDC group A and nine from CDC group B). In contrast to healthy control individuals, most patients displaying positive LPRs LPRs to HCMV had unstable responses. Sustained LPRs to HCMV were significantly associated with high pre-HAART nadir CD4(+) T cell counts. Long-term suppression of HIV viremia correlated with recovery of LPR to HCMV. Sequential PBMC cultures from most patients secreted IFN-gamma (but not IL-4) at normal levels upon HCMV stimulation, irrespective of the pre-HAART nadir CD4(+) T cell counts and CDC group to which patients belonged. Failure to reconstitute IFN-gamma response was associated with very low pre-HAART nadir CD4(+) T cell counts. Control of HCMV infection in the cohort was associated with either recovery or maintenance of IFN-gamma response rather than with reconstitution of LPR to HCMV. A LPR to HCMV was absent in three out of eight long term non-progressors; contrarily, all patients showed preserved IFN-gamma responses.

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Loss of cytomegalovirus (CMV) viraemia following highly active antiretroviral therapy in the absence of specific anti-CMV therapy

Cited by 96 publications

References 15 publications

Cytomegalovirus and HIV: A Dangerous Pas de Deux

Cytomegalovirus and HIV: A Dangerous Pas de Deux

Activity of antiretroviral drugs in human infections by opportunistic agents

Assessment of human cytomegalovirus specific T cell immunity in human immunodeficiency virus infected patients in different disease stages following HAART and in long‐term non‐progressors

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