Studies of viral co-factors for human immunodeficiency virus in vitro and in vivo.

Griffiths, Paul

doi:10.1099/0022-1317-79-2-213

Cited by 35 publications

(23 citation statements)

References 54 publications

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“…In the immunocompromised host, HHV-6 infection has been detected in the post-transplant period [Drobyski et al, 1993;Wilborn et al, 1994;Osman et al, 1996] and the virus has been associated with pneumonitis, marrow suppression, and encephalitis after bone marrow transplant [Cone et al, 1993;Drobyski et al, 1993Drobyski et al, , 1994. In addition, HHV-6 has been detected in autopsy samples in AIDS patients [Corbellino et al, 1993;Knox and Carrigan, 1994;Clark et al, 1996], and has been proposed as a possible co-factor, accelerating the progress of HIV disease [Griffiths, 1992;Lusso, 1996]. HHV-7 appears to cause some cases of exanthem subitum [Tanka et al, 1994;Torigoe et al, 1995], but otherwise has not been associated with particular diseases.…”

Section: Introductionmentioning

confidence: 96%

Human herpesviruses 6 and 7 as potential pathogens after liver transplant: Prospective comparison with the effect of cytomegalovirus

et al. 1999

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Because cytomegalovirus (CMV) is an important opportunistic infection after liver transplant, we conducted a prospective study to see if the same applied to human herpesviruses (HHV)-6 and -7. We used polymerase chain reaction (PCR) methods optimised to detect active, not latent, infection and studied patients not receiving antiviral prophylaxis for CMV. Post-transplant, 536 blood samples were tested by PCR (median 7; range 4-50). Active infection with CMV was detected in 28/60 (47%), HHV-6 in 19/60 (32%), and HHV-7 in 29/60 (48%) of patients. The PCR-positive samples were tested by quantitative-competitive PCR to measure the virus load of each betaherpesvirus. The median peak virus load for CMV was significantly greater than that for HHV-6 or HHV-7. Detailed clinicopathological analyses for the whole population showed that CMV and HHV-6 were each significantly associated with biopsy-proven graft rejection. Individual case histories suggested that HHV-6 and HHV-7 may be the cause of some episodes of hepatitis and pyrexia. It is concluded that HHV-6 is a previously unrecognized contributor to the morbidity of liver transplantation, that HHV-7 may also be important and that both viruses should be included in the differential diagnosis of graft dysfunction.

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Section: Introductionmentioning

confidence: 96%

Human herpesviruses 6 and 7 as potential pathogens after liver transplant: Prospective comparison with the effect of cytomegalovirus

et al. 1999

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“…Thus, there may be value in further evaluating the role of CMV in the disease progression of HIV and mortality. 28 Our study described a gradually later presentation of HIV infections in Singapore. In this era, our people still are not seeking early medical attention due to financial considerations and the social stigmata associated with the diagnosis of HIV in a traditionally and culturally conservative society.…”

Section: Discussionmentioning

confidence: 99%

The Epidemiology and Incidence of Cytomegalovirus Retinitis in the HIV Population in Singapore over 6 Years

Teoh¹,

Wang²,

Wong³

2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. We report the epidemiologic trend of cytomegalovirus (CMV) retinitis among human immunodeficiency virus (HIV) patients in Singapore.METHODS. Our study included a retrospective case series of HIV patients with newly diagnosed CMV retinitis (CMVR) at the Singapore CDC between 2005 and 2010. Demographics, symptoms, signs, and laboratory results, including CD4 counts, were collected. Prevalence and disease trends over time were measured. RESULTS.Of 224 new patients, 92.9% were male and 96.0% were on antiretroviral therapy (ART). Median age was 43.0 years, with a median CD4 count of 38.0 cells/lL at HIV diagnosis. There was a decline in CD4 counts at diagnosis, and median duration of ART initiation from HIV diagnosis generally was earlier. Overall incidence rate was 10.4 cases per 1000 person-years (PY) and the mortality rate was 19.4 per 1000 PY. Mean survival time was 160.2 months (95% confidence interval [CI] 150.3-170.2). The 25 patients who died during the study period were older at the time of CMVR diagnosis (P ¼ 0.003) and had lower CD4 counts (P ¼ 0.030). Worse prognoses were associated with older age (hazard ratio [HR] 1.06, 95% CI 1.02-1.10) and shorter time lag from HIV to CMVR diagnosis (HR 0.97, 95% CI 0.95-0.99). Patients who did not receive highly active antiretroviral treatment (HAART) had a higher mortality risk (HR 4.70, 95% CI 1.54-14.33).CONCLUSIONS. The incidence rate of CMVR was decreasing with earlier initiation of ART and lower CD4 counts at HIV diagnosis. Poor prognostic factors included older age, shorter time lag from HIV to CMVR diagnosis, and the absence of HAART. Constant ophthalmologic surveillance until immune reconstitution is recommended. (Invest Ophthalmol Vis Sci.

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“…These virus infections may cause disease in their own right, such as cytomegalovirus (CMV) retinitis, varicella zoster virus acute retinal necrosis, and herpes simplex virus esophagitis [Gallant et al, 1992;Pertel et al, 1992;Glesby et al, 1995]. In addition, it is theoretically possible that any of the herpesviruses may interact with HIV to accelerate the rate at which it causes immune deficiency [reviewed in Griffiths, 1992Griffiths, , 1998Lusso and Gallo, 1995].…”

Section: Introductionmentioning

confidence: 99%

Interactions between ?-herpesviruses and human immunodeficiency virus in vivo: Evidence for increased human immunodeficiency viral load in the presence of human herpesvirus 6

Emery

et al. 1999

J. Med. Virol.

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In vitro, beta-herpesviruses can stimulate or inhibit HIV replication under particular circumstances. In order to investigate the effects of beta-herpesvirus infection on HIV replication and vice versa at an organ level, we determined the quantitative relationships between cytomegalovirus (CMV), human herpesviruses (HHV) 6 and 7, and HIV-1 proviral DNA using quantitative competitive PCR methods in 141 organs collected at autopsy from 11 AIDS patients. The presence of HHV-6 DNA in an organ was significantly associated with elevated HIV-1 proviral DNA (difference in HIV median loads, 1.3 log10 genomes; P = 0.004). Consistent with this, there was a trend for the presence of HIV-1 proviral DNA to be associated with an elevated HHV-6 load (0.44 log10 difference; P = 0.07). In contrast, there were no significant differences between viral loads in the combinations of either CMV or HHV-7 with HIV-1 proviral DNA load. Pairwise combinations of the beta-herpesviruses revealed that the quantity of HHV-7 was increased in the presence of HHV-6 (difference in median loads, 1.3 log10; P = 0.001) and the quantity of HHV-6 was increased in the presence of HHV-7 (difference in median loads, 0.7 log10; P=0.002). These results demonstrate that the presence of HHV-6 in an organ is significantly associated with an elevated HIV-1 proviral load and have implications for understanding HIV pathogenesis in the human host and the role that beta-herpesviruses, especially HHV-6, might play as cofactors in the HIV disease process.

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Studies of viral co-factors for human immunodeficiency virus in vitro and in vivo.

Cited by 35 publications

References 54 publications

Human herpesviruses 6 and 7 as potential pathogens after liver transplant: Prospective comparison with the effect of cytomegalovirus

Human herpesviruses 6 and 7 as potential pathogens after liver transplant: Prospective comparison with the effect of cytomegalovirus

The Epidemiology and Incidence of Cytomegalovirus Retinitis in the HIV Population in Singapore over 6 Years

Interactions between ?-herpesviruses and human immunodeficiency virus in vivo: Evidence for increased human immunodeficiency viral load in the presence of human herpesvirus 6

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