Disease relevance of Viremia

• All of them had either HIV p24 antigenemia or plasma viremia and CD4-lymphocyte counts of 200 to 500 per cubic millimeter when they began treatment [1].
• HIV-1 viremia prevents the establishment of interleukin 2-producing HIV-specific memory CD4+ T cells endowed with proliferative capacity [2].
• A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies [3].
• We conclude that verapamil, whether given before infection or after peak viremia in an encephalomyocarditis model of murine myocarditis, significantly reduces the microvascular changes and myocardial necrosis, fibrosis, and calcification leading to cardiomyopathy [4].
• Resolution of hepatitis C viremia was significantly more likely in patients who developed HCV-specific T-cell proliferation with increased IFN-gamma production [5].

High impact information on Viremia

• The reduction in viremia correlated with the levels of hyperglucosylated glycan in the serum of treated animals [6].
• In viremic patients the presence of IFN-gamma-producing cells was restricted to periods of elevated viremia [2].
• These observations may explain the failure of AZT therapy to clear viremia, consistent with the presence of a drug-resistant reservoir of infected cells in vivo [7].
• MHC class II genotype and the control of viremia in HIV-1-infected individuals on highly active antiretroviral therapy [8].
• This therapeutic regimen resulted in a remarkable increase in the number of CD4+ cells and in the prolonged reduction of the levels of viremia [9].

Chemical compound and disease context of Viremia

• Group 2 mice received only verapamil orally starting on day 4 after infection, coincident with peak viremia [4].
• Interferon alone (P < 0.05) or with ribavirin (P < 0.01) significantly decreased the viral population, resulting in sustained loss of viremia with normal enzyme levels in 2 of 9 and 3 of 9 patients, respectively, in each therapy during follow-up [10].
• Independent predictors of sustained response were undetectable viremia at the first month of therapy (P < 0.001), undetectable viremia at the third month (P < 0.001), younger age (P = 0.006), nonsporadic infection (P = 0.012), and higher pretreatment aspartate aminotransferase levels (P = 0.032) [11].
• 3-year suppression of HIV viremia with indinavir, zidovudine, and lamivudine [12].
• We treated 12 patients who had acquired immunodeficiency syndrome and active HTLV-III/LAV viremia with suramin, a potent competitive inhibitor of reverse transcriptase, in six weekly induction doses of 1 g, followed by weekly maintenance doses of 500 mg [13].

Biological context of Viremia

• Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production [3].
• In contrast, a decrease in virus replication in lymph nodes was observed in four of six patients who added didanosine to their regimen, and this was associated with a decrease in plasma viremia [14].
• High-titer viremia (108 to 109 genome equivalents per ml) and transiently elevated serum alanine transaminase activities were present from weeks 4 to 12 postinoculation in both animals [15].
• The amounts of viremia and the distribution of viruses were analyzed by spot hybridization, polymerase chain reaction, restriction fragment length polymorphism, cloning and sequencing [16].
• When HCV infection occurs in immunocompromised hosts, antibody formation against core, NS3, or NS4 antigens may be weak in the presence of HCV viremia and cannot be detected by routine anti-HCV tests [17].

Anatomical context of Viremia

• There was a significant positive correlation between the level of viremia 18 hr after infection and the sialic acid content of the host's erythrocytes [18].
• We conclude that HCV RNA was detected by IS-RT-PCR in 0 to 35% of hepatocytes in patients with chronic HCV infection, detection of HCV RNA in liver by IS-RT-PCR was associated with higher viremia levels and IFN-alpha therapy reduced hepatocytic expression of HCV RNA [19].
• Immunization with a modified vaccinia virus expressing simian immunodeficiency virus (SIV) Gag-Pol primes for an anamnestic Gag-specific cytotoxic T-lymphocyte response and is associated with reduction of viremia after SIV challenge [20].
• Polymerase chain reaction for CMV DNA in leukocytes had the best positive and negative predictive values for the development of disease within 2 months from transplantation, and shell-vial or tube culture viremia was the best predictor thereafter [21].
• In individuals with HIV-1 viremia, there was a direct correlation between the level of expression of p58.1, p58.2, and CD94 receptors and plasma HIV viremia, suggesting that ongoing active HIV replication has an effect on the expression of such receptors on NK cells [22].

Gene context of Viremia

• Previous studies have demonstrated that the expression of CD38 on CD8+ T cells is associated with poor prognostic outcome in infected individuals with detectable plasma viremia; however, the relationship between the expression of CD38 and the frequency of HIV-specific CD8+ T cells is unclear [23].
• Since an efficient control of virus infections may depend on the appropriate lymphokine profile, we studied cytokine responses and CD30 induction, a recently proposed surrogate marker of type 2 cells, in 10 healthy anti-hepatitis C virus (HCV)-seropositive blood donors without viremia (group A) and in 15 patients with hepatitis C (group B) [24].
• CCR5, GPR15, and CXCR6 are major coreceptors of human immunodeficiency virus type 2 variants isolated from individuals with and without plasma viremia [25].
• In certain mouse strains, a single host gene, Rfv3, controls the ability to mount a virus-specific neutralizing antibody response which results in elimination of viremia [26].
• APOBEC3F and APOBEC3G mRNA levels do not correlate with human immunodeficiency virus type 1 plasma viremia or CD4+ T-cell count [27].

Analytical, diagnostic and therapeutic context of Viremia

• Whereas sera from mice treated with OK-432 were the only positive for interferon, viremia was clearly demonstrated in control groups by reverse transcriptase assays of the plasma [28].
• METHODS: Viremia was assayed in virus-infected and control patients using the polymerase chain reaction and Southern blotting [29].
• Passive immunotherapy of new born BALB/Mo mice with anti-gp70 glycoprotein or anti-M-MuLV serum prevented viremia and delayed significantly the subsequent development of leukemia [30].
• Retrospective analysis of HHV-8 viremia and cellular viral load in HIV-seropositive patients receiving interleukin 2 in combination with antiretroviral therapy [31].
• To define the duration of viremia in the course of acute hepatitis B, we semiquantitatively determined the levels of hepatitis B virus (HBV) DNA in the sera, using polymerase chain reaction (PCR) coupled with Southern blotting, of non-immunocompromised patients with self-limited acute hepatitis B [32].

References