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PubMed2005

Hepatic steatosis in HIV/hepatitis C coinfection: prevalence and significance compared with hepatitis C monoinfection.

Liver disease in patients coinfected with HIV and hepatitis C virus (HCV) has received increasing attention in recent years. Steatosis is accepted as an important contributor to liver disease in patients with HCV, but despite coinfected patients having several reasons to have steatosis, the prevalence and significance of such changes has received scant attention. We examined steatosis in an unselected cohort of coinfected patients and compared its prevalence and predictors with findings in monoinfected patients, where these relationships have been established. We studied 92 coinfected and 372 monoinfected patients undergoing staging liver biopsy. Baseline characteristics of the two groups differed significantly, pointing at different contributors to steatosis in each. Histological inflammation and fibrosis were very similar in the two groups, but steatosis was less in coinfected patients. Steatosis had a univariate association with fibrosis in both groups, but retained a multivariate association only in monoinfected patients. Other multivariate predictors of steatosis in monoinfected patients were the accepted variables of elevated body mass index, male sex, and genotype 3a infection, as well as age. In coinfected patients, however, age was the only multivariate predictor. Undetectable HIV viral load was associated with steatosis in coinfected patients in univariate analysis, but highly active antiretroviral therapy or its individual components could not be initially linked to steatosis. In conclusion, steatosis is less common in HIV/HCV coinfected patients than similar HCV monoinfected patients, and predictors of steatosis differ between the two groups.

Adult↗

PubMed1991

Altered HIV expression and EBV-induced transformation in coinfected PBLs and PBL subpopulations.

Human immunodeficiency virus (HIV) IIIB expression and Epstein-Barr virus (EBV) B95.8-induced transformation were studied during coinfection. Coinfection of peripheral blood lymphocyte (PBL) cultures with HIV and EBV resulted in down-regulation of HIV expression. EBV-induced and spontaneous transformation were markedly reduced in PBL cultures exposed to HIV before EBV. On the other hand, transformation was enhanced when PBL cultures were infected with HIV either simultaneous to or after EBV. Reconstitution of EBV-infected B cell cultures with autochthonous T cells demonstrated that HIV-infected T cells had a reduced ability to inhibit EBV-induced transformation. PHA stimulation of HIV-infected T cells eliminated their ability to inhibit EBV-induced transformation. Lymphoblastoid cell lines (LCLs) established from coinfected PBLs expressed B cell markers and were EBV positive, while a large proportion of the LCLs expressed HIV antigens, released reverse transcriptase activity into the supernatant, and produced syncytia when cocultivated with indicator cell line SupT1. HIV provirus could be detected in LCLs established from coinfected cultures by PCR amplification using specific sets of amplimers for gag and env genes of HIV. To more closely examine the role of various cell types in lymphocyte transformation and HIV replication during coinfection, experiments were carried out using subpopulations enriched for either B or T cells. Simultaneous coinfection of purified B cells with EBV and HIV resulted in a marked reduction of HIV expression, whereas EBV-induced transformation was enhanced. In contrast, spontaneous B cell transformation was inhibited by HIV. A proportion of LCLs established from purified B cells coinfected with EBV and HIV expressed HIV antigens, released reverse transcriptase activity, and produced syncytia on SupT1 cells. These results demonstrate that the IIIB strain of HIV and B95.8 strain of EBV can interact during coinfection of B cells to alter the course of virus expression.

B-Lymphocytes↗

PubMed1996

Responsiveness to interferon alpha treatment in patients with chronic hepatitis C coinfected with hepatitis G virus.

BACKGROUND/AIMS: Patients with chronic hepatitis C are often coinfected with the new identified Flaviviridae-like agent, termed hepatitis G virus (HGV). The aim of the study was to investigate the responsiveness of hepatitis G virus to interferon alpha and to evaluate whether a hepatitis G virus coinfection negatively influences the outcome of treatment in chronic hepatitis C. METHODS: One hundred and fifteen patients with histologically proven chronic hepatitis C were treated with interferon alpha and investigated for the presence of hepatitis G virus coinfection by nested polymerase chain reaction with primers from the helicase region of hepatitis G virus. All patients received at least 3 MU (range 3-6) interferon alpha thrice weekly for at least 6 months (mean 8, range 6-12). Polymerase chain reaction products of seven pre- and post-treatment hepatitis G virus positive patients were directly sequenced for identification of sequence variability during the follow-up. RESULTS: Eighteen (16%) patients were coinfected with hepatitis G virus. Although nine (50%) of these patients became HGV RNA negative during interferon alpha therapy, only three patients (17%) remained HGV RNA negative at the end of follow-up (mean 24 months). The rate of sustained response of chronic hepatitis C was not significantly different between patients with hepatitis C virus infection and HCV/HGV coinfection (19% vs 28%). Severity of liver disease as determined by alanine aminotransferase levels, histology and hepatitis C virus viremia was not significantly different in patients with hepatitis C virus or HCV/HGV coinfection. Sequence analysis of the helicase region revealed that our isolates all belonged to the hepatitis G virus and not to the GBV-C like genotype. No amino acid exchanges during the observation period of up to 48 months were observed, indicating that this region is highly conserved. CONCLUSIONS: The responsiveness of hepatitis G virus to interferon alpha in chronic HCV/HGV coinfected patients is similar to that observed in chronic hepatitis C. Hepatitis G virus coinfection seems not to interfere with the efficacy of interferon alpha treatment in patients with chronic hepatitis C.

Adult↗

PubMed2004

Low-level hepatitis C viremia and humoral immune response to NS4 in chronic hepatitis B virus-hepatitis C virus coinfection.

BACKGROUND: There is a limited amount of published data on the interference of hepatitis B virus (HBV) on hepatitis C virus (HCV). The aim of this study was to investigate the effect of concurrent HBV infection on serum titers of HCV RNA and HCV antibody profiles in chronic HCV infection. METHODS: The clinical and virological profiles (serum titers of HCV RNA, HCV genotypes and antibody profiles) of 25 patients with chronic HBV-HCV coinfection were compared with those of 25 age- and sex-matched patients with HCV infection alone. RESULTS: Among the 25 patients with HBV-HCV coinfection, only 3 were found hepatitis Be antigen (HBeAg) and HBV DNA positive by hybridization assays, and the other 11 were found HBV DNA positive by polymerase chain reaction. Genotype 1b was dominant in both HBV-HCV coinfection and HCV infection alone (64% versus 84%, P > 0.1). Patients with HBV-HCV coinfection had significantly lower alanine aminotransferase (ALAT) levels and inflammatory scores but higher fibrosis scores than those with HCV infection alone. Serum titers of HCV RNA were significantly lower in HBV-HCV coinfection than in HCV infection alone. The frequency and relative intensity of antibody response to core, E2/NS1, NS3, and NS5 showed no significant difference between the two groups, but antibody response to NS4 was diminished significantly in HBV-HCV coinfection. CONCLUSIONS: In HBV-HCV coinfection, serum levels of HBV DNA are usually low or undetectable. Concurrent HBV infection, however, could interfere with HCV replication and suppress antibody response to NS4. The biological significance of selective inhibition of humoral immune response to NS4 in HBV-HCV coinfection should be further studied.

DNA, Viral↗

PubMed1997

Comparative histologic features of liver biopsy specimens from patients coinfected with hepatitis G and C viruses with chronic hepatitis C virus alone: an age-, sex-, disease duration-, and transmission-matched controlled study of chronic hepatitis.

Hepatitis G virus (HGV) is a recently described, parenterally spread, positive-strand RNA virus of the Flaviviridae family. There is a high rate of HGV coinfection in patients with hepatitis C virus (HCV). Whether HGV can cause or is pathogenetically related to clinically apparent chronic liver disease, or whether HGV alters the course of hepatitis C in patients who are coinfected with both viruses is unknown. We studied 13 biopsy specimens from 11 patients coinfected with HGV and HCV and compared them with 15 biopsy specimens from a group of patients infected only with HCV who were matched for age, sex, disease duration, and transmission mode to characterize the histologic features of coinfected liver biopsy specimens and to look for any histologic features that might allow identification of coinfected patients. Three of the biopsy specimens from coinfected patients had a modified histologic activity index score of minimal chronic hepatitis, three of mild, two of mild/moderate, and five of moderate chronic hepatitis. Bile duct injury was absent in seven specimens, minimal in five, and mild in one. The biopsy specimens from patients who were coinfected with HGV and HCV had similar histologic features to the biopsy specimens of patients infected with HCV alone. There were no detectable histologic differences between the biopsy specimens from the two patient groups. The P values for the statistical comparisons confirmed this impression. In addition, no group of histologic features distinguished the coinfected patient group from the control group. Any suspicion that a clinician might have about the presence of HGV requires confirmation by reverse transcriptase-polymerase chain reaction testing of serum samples. Our results suggest that HGV most likely does not actively participate in the cytotoxic effects of chronic hepatitis or does so by a mechanism as yet undefined. Although HGV can cause chronic infection, the present study provides no evidence that it causes or contributes to chronic hepatitis.

Biopsy↗

PubMed1997

HIV viral load and CD4+ lymphocyte counts in subjects coinfected with HTLV-I and HIV-1.

Reports indicate that there is a dissociation between markers of HIV disease progression and clinical stage among subjects coinfected with human T-cell lymphotropic virus type I (HTLV-I) and HIV. HTLV-I coinfection does not appear to affect HIV viral load, currently considered to be the best marker of HIV disease progression. We measured HIV RNA levels in stored serum samples from 23 subjects with coinfection and 92 subjects with HIV single infection and examined the correlation with the CD4+ lymphocyte count. Subjects were recruited from an ongoing HIV cohort study in Rio de Janeiro, Brazil. In both groups, CD4+ lymphocyte counts declined with increasing levels of HIV RNA. In a linear regression analysis adjusting for HIV RNA serum level, coinfected individuals had an estimated 78% higher CD4+ lymphocyte count than those with single infection. Simultaneous adjustment for beta2-microglobulin level increased the difference, with coinfected individuals having 146% (p = 0.005, 95% CI: 32% to 359%) higher CD4+ counts. These data suggest that the higher CD4+ lymphocyte counts associated with coinfection do not provide immunologic benefit and may reflect HTLV-I-associated nonspecific lymphocyte proliferation. The results of this and other studies suggest that the CD4+ count cutoff values used in making clinical decisions in HIV infection may not be appropriate in coinfection. As with HIV single infection, HIV virus load may be the optimal surrogate marker for subjects with coinfection.

Acquired Immunodeficiency Syndrome↗

PubMed2006

Rates and predictors of hepatitis C virus treatment in HCV-HIV-coinfected subjects.

BACKGROUND: True treatment rates and the impact of comorbidities on treatment rates for hepatitis C virus in the HCV-HIV-coinfected subjects are unknown. AIM: To quantify the rates of treatment prescription and the effect of comorbidities on hepatitis C virus treatment rates in HCV-HIV-coinfected veterans. METHODS: The Veterans Affairs National Patient Care Database was used to identify all hepatitis C virus-infected subjects between 1999 and 2003 using ICD-9 codes. Demographics, comorbidities and pharmacy data were retrieved. We used logistic regression to compare the predictors of hepatitis C virus treatment in hepatitis C virus-monoinfected and HCV-HIV-coinfected subjects. FINDINGS: We identified 120 507 hepatitis C virus-infected subjects, of which 6502 were HIV coinfected. 12% of the hepatitis C virus-monoinfected and 7% of the -coinfected subjects were prescribed hepatitis C virus treatment (P < 0.0001). Those not prescribed treatment were older (48.6 years vs. 47.7 years, P = 0.007) and more likely to be black (52% vs. 32%, P < 0.0001). HIV coinfected was less likely to be prescribed hepatitis C virus treatment (OR 0.74, 95% CI: 0.67-0.82). Among the coinfected subjects, the following were associated with non-treatment (OR, 95% CI): black race (0.45, 0.35-0.57); Hispanic race (0.56, 0.38-0.82); drug use (0.68, 0.53-0.88); anaemia (0.17, 0.11-0.26); bipolar disorder (0.63, 0.40-0.99); major depression (0.72, 0.53-0.99); mild depression (0.47, 0.35-0.62). CONCLUSIONS: A small number of HCV-HIV-coinfected veterans are prescribed treatment for hepatitis C virus. Non-treatment is associated with increasing age, minority race, drug use and psychiatric illness. Further studies are needed to determine the eligibility for treatment and reasons for non-treatment for hepatitis C virus.

Cohort Studies↗

PubMed1998

Effects of hepatitis G virus coinfection on severity of hepatitis C: relationship to risk factors and response to interferon treatment.

The aims of the present study were to identify characteristics that are more often associated with hepatitis G virus (HGV) coinfection in Australian patients infected with the hepatitis C virus (HCV) and to investigate the effects of HGV on the histological and functional severity of chronic hepatitis C. Serum samples from 209 patients with chronic hepatitis C were tested for HGV-RNA using single-round reverse transcriptase-polymerase chain reaction to primers directed at the NS5 region of the HGV genome. Hepatitis G virus RNA was detected in 40 cases (19%). Hepatitis G virus-coinfected patients tended to be younger and parenteral risks could be identified in all but six. Although country of birth did not differ significantly between the coinfected and HCV-alone groups, HGV-positive patients appeared to be less likely to have originated from Asia. On logistic regression analysis, HCV genotype 3a was found in a significantly higher proportion of patients with HGV coinfection than other genotypes (P < 0.01). Liver histology and response to interferon were similar in the HGV-coinfected and HCV-alone groups and liver-related complications appeared to occur less frequently in patients with both HGV and HCV. On univariate analysis, antipyrine clearance was found to be higher in the coinfected group (P < 0.05), implying better preservation of hepatic metabolic function, but this difference was lost when adjusted for HCV genotype. In conclusion, coinfection with HGV was more commonly associated with HCV genotype 3a, a genotype associated with injection drug use in younger patients. However, the presence of HGV coinfection did not adversely affect liver disease or the response to interferon treatment in patients with chronic hepatitis C.

Adult↗

PubMed2005

The effect of HIV coinfection on the risk of cirrhosis and hepatocellular carcinoma in U.S. veterans with hepatitis C.

OBJECTIVES: This study was conducted to determine whether HIV coinfection increases the risk of cirrhosis in HCV-infected patients in the HAART and pre-HAART eras. Further, the risk of hepatocellular carcinoma was also examined. METHODS: This retrospective cohort study was conducted among HCV-infected veterans who were seen at one of the 172 Veterans Health Administration hospitals between October 1, 1991 and September 30, 2000. Patients with prerecorded advanced liver disease were excluded. Incidence rates, cumulative incidence, and Cox proportional hazard ratios were calculated. RESULTS: There were 26,641 patients with HCV-only and 4,761 patients with HCV-HIV coinfection. The unadjusted incidence rate of cirrhosis was lower in patients with coinfection than HCV-only (p < 0.01). After controlling for demographics and confounders (including alcoholism and chronic hepatitis B), coinfection was not significantly associated with cirrhosis. However, there was an increased risk of cirrhosis in patients with coinfection compared to HCV-only during the pre-HAART era (before October 1, 1996) (hazard ratio = 1.48, 1.06-2.07, p= 0.02), but not among patients who entered the cohort during the HAART era. The unadjusted incidence rate of hepatocellular carcinoma in patients with coinfection and HCV-only was 1.3 and 2/1,000 person-years, respectively (p= 0.04). In the multivariate model, coinfection was not associated with hepatocellular carcinoma (hazard ratio = 0.84, p= 0.40). CONCLUSIONS: Coinfection was a significant risk factor for cirrhosis only during the pre-HAART era and was not associated with hepatocellular carcinoma, irrespective of time period.

Adult↗

PubMedDate not supplied

[Prevalences of hepatitis virus coinfection and indications for chronic hepatitis C virus treatment and liver transplantation in Spanish HIV-infected patients. The GESIDA 29/02 and FIPSE 12185/01 Multicenter Study].

INTRODUCTION: The aims of this study were to estimate the prevalence of HIV and hepatitis virus coinfection in the Spanish population and to determine the percentage of patients who are candidates for chronic hepatitis C virus (HCV) treatment and liver transplantation within this population. METHODS: A cross-sectional study was performed in 2002 in two Spanish populations of HIV-infected patients: 1,260 patients from 39 centers throughout Spain (P1) and 1,560 patients from three tertiary teaching hospitals in Madrid (P2). RESULTS: The following hepatitis A virus (HAV), hepatitis B virus (HBV) and HCV serological prevalence were found in the P1 and P2 groups, respectively: HAV-IgG antibodies: 74% and 78%; HBsAg1: 4.9% and 4.8%; HBsAg-, anti-HBc1, anti-HBs1: 39% and 39%; HBsAg-, anti-HBc1, anti-HBs-: 25% and 31%; HBsAg-, anti-HBc-, anti-HBs1: 7% and 8%; HBsAg-, anti-HBc-, anti-HBs-: 22% and 16%. Anti-HCV1: 61% and 65%, respectively. Of the patients with positive HCV serology, 88.8% and 84.6% of each group were positive for HCV-RNA by polymerase chain reaction. Multiple coinfections with hepatitis viruses were found in 3.2% and 2.8%, respectively; of these, 70% and 78% had coinfection with HBV, HCV and HDV. Liver cirrhosis was found in 5.8% and 9.6% of the patients coinfected with HIV and HCV, respectively. Liver transplant was indicated in approximately one out of every six coinfected patients with liver cirrhosis. The 43 and 37% of the HCV coinfected patients were good candidates for anti-HCV treatment, but only 14% and 15% of patients had initiated it. CONCLUSIONS: A high percentage of HIV-infected patients in Spain were coinfected with hepatitis viruses, especially HCV. The number of possible candidates for liver transplantation is rising and could increase in the next few years. In the future, greater efforts to treat HIV-and hepatitis virus-coinfected patients will be required.

Adult↗

PubMed2006

[Early virologic response value as predictive factor of sustained virologic response to treatment with interferon alpha-2b plus ribavirin in chronic hepatitis C patients with or without HIV coinfection].

BACKGROUND AND OBJECTIVE: The most effective currently available therapy for chronic hepatitis C virus infection is the combination of interferon alpha-2b plus ribavirin both, in patients with human immunodeficiency virus (HIV) coinfection and in patients without coinfection. In an attempt to avoid morbidity and health costs we searched for an indicator of early virologic response (EVR). We evaluated the EVR efficiency at 4 and 12-weeks after the initiation of antiviral combination therapy. PATIENTS AND METHOD: A total of consecutive 127 patients with chronic hepatitis C virus infection treated with combination therapy for 12 months in genotypes 1 and 4 and for 6 months in genotypes 2 and 3, were studied, 62 HIV-coinfected and 65 non-coinfected. They were evaluated for sustained virologic response and EVR at 4 and 12-weeks to initial therapy. RESULTS: Sustained virologic response was greater in the non-coinfected group than coinfected group; these differences were significant for genotypes 1 and 4. In both groups EVR had a 100% predictive negative value at 12-weeks after the initiation of therapy in genotypes 1 and 4, however came down in 79% at 4-weeks. CONCLUSIONS: The EVR at 12-weeks after the initiation of therapy has a 100% predictive negative value in coinfected and non-coinfected patients. Patient adherence to prescribed antiviral therapy is a predictive value of response.

Adult↗

PubMed2005

Evolution of virulence: coinfection and propagule production in spore-producing parasites.

BACKGROUND: The evolution of within-host growth rates by parasites is expected to depend on a trade-off between propagule production and virulence. The presence of coinfections, however, is thought to alter this trade-off, and hence alter the evolutionarily stable strategy (ESS) for the parasite. Here I consider a model wherein the number of coinfections that are identical by descent can depend on the parasite's reproductive strategy. Transmission success was treated as being either a negative-linear or a negative-exponential function of the total number of propagules produced by all coinfections. RESULTS: Increasing the number of unrelated coinfections either selected for a decrease in reproductive output by the parasite (linear case), or had no effect on the ESS (exponential case). Nonetheless, the total number of propagules produced within each host increased in both cases. Increasing the relatedness among coinfections, however, selected for reductions in parasite reproduction in both cases. CONCLUSION: Unrelated coinfection may increase overall parasite virulence, but the result stems from adding more infections rather than to more aggressive growth by the individual infections. However, all else being equal, if the coinfections are more related than expected by chance alone, then the total reproductive output by all coinfections would be expected to be reduced, resulting in reduced virulence.

Adaptation, Biological↗

PubMedDate not supplied

Low incidence of severe liver events in HIV patients with and without hepatitis C or B coinfection receiving lopinavir/ritonavir.

OBJECTIVES: To analyze the incidence of severe liver events in HIV patients treated with lopinavir/ritonavir and the role of coinfection in the development of this toxicity. METHOD: This was a retrospective, multicenter, cohort study of all HIV-positive patients who started a regimen of HAART that included lopinavir/ritonavir (LPV/r). The main outcome variable was the emergence of a severe liver event, defined as decompensation of pre-existing chronic liver disease and grade 3-4 hypertransaminasemia (HT), that is, plasma AST or ALT values >5 times above the upper limit of normality, if baseline levels were normal, or >3.5 times the baseline values when they were abnormal. RESULTS: 388 HIV-infected patients were included, with a median follow-up of 25.6 months. Coinfection with HCV was present in 61% of the patients and with HBV in 6.7%. There were 6 cases of severe liver events, all involving patients who were coinfected with HCV and all within the first 6 months. This represents 0.72 events per 100 patient-years (95% confidence interval [CI] 0.36-2.98) and 1.21 events per 100 patient-years (95% CI 0.60-5.86) in coinfected patients. The only factors associated with severe liver events at 6 months were baseline HT and HCV coinfection. CONCLUSION: The incidence of severe hepatic events in HIV-positive patients receiving a HAART regimen including LPV/r was very low, even in coinfected patients. HCV coinfection and baseline HT were the only factors associated with severe liver events. LPV/r can be considered a safe and well-tolerated option in HIV patients with hepatotropic virus coinfections.

Adult↗

PubMed2002

Hepatitis C virus infection in children coinfected with HIV: epidemiology and management.

Mothers with hepatitis C virus (HCV) and HIV coinfection are the major source of HCV/HIV coinfection in infancy and childhood. There is no known intervention capable of interrupting HCV spread from mother to child, while the majority of infant HIV infections occurring in the developed world can be prevented by antiretroviral prophylaxis in the mother and child, elective caesarean section, and formula-feeding. In the era preceding treatment of HIV infection with highly active antiretroviral therapy, HCV coinfection was of little concern because the short-term survival of patients with HIV infection prevented the slowly developing consequences of chronic hepatitis C. As the life expectancy of patients with HIV infection increased with therapy, HCV has emerged as a significant pathogen. Several lines of evidence in adult patients suggest that liver disease may be more severe in patients coinfected with HIV and that progression of HIV disease may be accelerated by HCV coinfection. Whether coinfected children may share these clinical patterns remains a matter of speculation. Chronic hepatitis C in otherwise healthy children is usually a mild disease; liver damage may be sustained and fibrosis may increase over the years, suggesting slow progression of the disease. Interferon-alpha has been the only drug used in the past decade to treat hepatitis C in children and adolescents, with average response rates of 20%. Preliminary results of treatment with interferon-alpha and ribavirin suggest that the efficacy would be greater with combined therapy. These treatment protocols have not yet been applied to children coinfected with HIV, but the increasing number of long-term survivors will probably prompt further investigation in the near future. At present, treating HIV disease and monitoring HCV infection and hepatotoxicity induced by antiretroviral drugs seem to be the more reasonable approach to HCV/HIV coinfection in childhood.

Child↗

PubMed1999

HIV-HCV RNA loads and liver failure in coinfected patients with coagulopathy.

BACKGROUND AND OBJECTIVE: The aim of this study was to measure contemporaneously HCV-RNA load, HIV-RNA load and CD4+ lymphocyte count in HCV/HIV coinfected patients with coagulopathy and to examine the relationship between these parameters and the liver failure. DESIGN AND METHODS: A cross-sectional study was performed on 54 patients with severe coagulopathy: 39 HCV/HIV coinfected and 15 HCV+/HIV- comparable for age and HCV exposure time. HCV-RNA and HIV-RNA load, CD4+ lymphocyte count, biochemical and ultrasonographic parameters were evaluated at the time of entry to the study. RESULTS: Mean HCV-RNA load was significantly higher in coinfected patients (643,872 717,687 copies/mL) than in HCV+/HIV- (mean 161,573 276,896 copies/mL) (p = 0.01). The 39 HCV/HIV coinfected patients had a mean HIV-RNA load of 205,913 456,311 copies/mL (range 4,000-2,500,000) and a mean CD4+ lymphocyte count of 206.5171/microL (range 5-693). Five of the 39 (12.8%) coinfected patients had liver failure. In these five patients the mean HCV-RNA load (770,200 996,426 copies/mL) was high but not significantly different from that in the 34 HCV+/HIV+ patients (623,496 682,239 copies/mL) without liver failure (p = 1.0). Coinfected patients with liver failure had a significantly higher HIV-RNA load (mean 764, 599 978,542 copies/mL) and lower CD4+ lymphocyte count (mean 52.655. 6/microL) than those observed in coinfected patients without liver failure (p = 0.007 and p = 0.03, respectively). A significant inverse correlation was found between CD4+ lymphocyte count and HIV-RNA load (r = -0.37, p = 0.01). INTERPRETATION AND CONCLUSIONS: HCV-RNA load is significantly higher in HIV+ than in HIV- patients with coagulopathy. Liver failure was found only in the HCV/HIV coinfected patients with severe immunodepression, expressed either by low CD4+ lymphocyte count or by high HIV-RNA load.

Adult↗

PubMed2001

[Effects of hepatitis G virus coinfection on hepatic pathological changes of patients with chronic hepatitis B: a long-term comparative study].

OBJECTIVE: To observe the long-term effect of hepatitis G virus (HGV) coinfection on hepatic pathological changes of patients with chronic hepatitis B (CHB) and explore the pathogenicity of HGV. METHODS: Menghini method liver biopsy was performed on 45 patients with CHB twice with an interval of 5 years on a voluntary basis. The liver tissue of 21 cases was HGV nonstructural region 5 (HGV NS5) antigen positive by peroxidase anti-peroxidase (PAP) immunohistochemical staining assay (HGV coinfection group) in these two tests, and 24 cases were negative (HGV noncoinfection group). There was no significant difference in age, sex, course of disease, amount of serum HBV-DNA by competitive quantitative polymerase chain reaction assay and severity of hepatic pathological leisions between these two groups (P < 0.05) and they were treated with the same scheme and without sustained curative effeect. The hepatic pathological changes of the two groups after 5 years were compared and analysed retrospectively. RESULTS: There was no significant difference in basic hepatic pathological change, severity of inflammatory activity grade and fibrosis stage in these two groups. The numbers of cases of inflammatory activity grade G1, G2, G3, and G4 were 3, 7, 7, and 4 in HGV coinfection group, and 5, 8, 7, and 4 in HGV noncoinfection group in the beginning of observation; and were 3, 5, 7, and 6 in HGV coinfection group, and 4, 6, 8, and 6 in HGV noncoinfection group after 5 years. The numbers of cases in fibrosis stages S1, S2, S3, and S4 were 4, 7, 7, and 3 in HGV coinfection group, and 6, 8, 6, and 4 HGV noncoinfection group in the beginning of observation; and were 3, 6, 5, 7 in HGV coinfection group, and 4, 7, 5, and 8 in HGV noncoinfection group after 5 years (P > 0.05). CONCLUSION: HGV coinfection does not lead to the activation of hepatic pathological changes and does not speed up the progression of fibrosis in patients with CHB. HGV coinfection does not play an obvious role in long-term hepatic pathological changes of patients with CHB. HGV has at most a mild hepatic pathogenicity.

Adult↗

PubMed2004

[Clinical, epidemiological and immunological study of patients coinfected with HIV and HTLV-1].

We studied the prevalence of antibodies against HTLV-1 among every HIV-infected outpatients assisted in our hospital between January 1st 2000 and June 30th 2003. We reviewed the epidemiological data, clinical findings, viral load and CD4 cells-count, comparing coinfected with non HTLV-1 coinfected. We found a prevalence of HTLV-1 infection of 8.1% (23/282); 8.5% (12/141) in men and 7.8% (11/141) in women [[OR=0.91 (0.36<OR<2.3) p=0.8]; 12.4% (16/129) among patients users of illicit drugs and 4.6% (7/152) among non-users [OR=2.93 (1.09<OR<8.17) p=0.03]; 20.8% (16/77) in injecting drugs users (IDU) and 3.4% (7/205) in non-IDU patients [p=0.000006 OR=7.42 (2.71<OR<20.9)]. Ninety six patients (96/282) had history of AIDS defining diseases (ADD). No differences in the ADD were found among coinfected and no coinfected patients. No patient developed any disease relative to HTLV-1. The mean of CD4-cells among HTLV-1 coinfected with history of ADD naïve patients (n=7) was 211 cells/ml, and 87.9 cells/ml among those not-coinfected (n=55) [t-test=2.82; p=0.006]. The viral load was similar among every investigated group of patients. We found a high prevalence of HTLV-1 infection in HIV-infected patients (higher among IDU). The CD4-cell count of patients suffering from an AIDS defining disease was higher among HTLV-1/HIV coinfected patients than in singly HIV infected, this could show a grade of missfunction of CD4-cells in coinfected patients.

Adolescent↗

PubMed1998

Evolution of virulence: a unified framework for coinfection and superinfection.

Models of the evolution of parasite virulence have focused on computing the evolutionarily stable level of virulence favored by tradeoffs within a host and by competition for hosts, and deriving conditions under which strains with different virulence levels can coexist. The results depend on the type of interaction between disease strains, such as single infection (immunity of infected individuals to other strains), coinfection (simultaneous infection by two strains), and superinfection (instantaneous takeover of host by the more virulent strain). We present a coinfection model with two strains and derive the superinfection model as the limit where individuals are rapidly removed from the doubly-infectious class. When derived in this way, the superinfection model includes not only the takeover of hosts infected by the less virulent strain, but new terms which take into account the possibility of increased mortality of doubly-infected individuals. Coinfection tends to favor higher virulence and support more coexistence than the single infection model, but the detailed results depend sensitively on two factors: (1) whether and how the model is near the superinfection limit, and (2) the shape of the coinfection function (the function describing the rate at which a more virulent strain can infect a host). If the superinfection limit arises due to rapid mortality of doubly-infected hosts, there is a region of uninvadable virulence levels rather than coexistence. When the coinfection function is discontinuous, as in many previous models, neither the coinfection model nor the superinfection limit can support an evolutionarily stable virulence level. Piecewise differentiable and differentiable coinfection functions produce qualitatively different results, and we propose that these more general cases should be used to study evolution of virulence when other mechanisms like space, population dynamics, and stochasticity interact.

Animals↗