scholarly journals Impact of Heterozygosity for the Chemokine Receptor CCR5 32‐bp‐Deleted Allele on Plasma Virus Load and CD4 T Lymphocytes in Perinatally Human Immunodeficiency Virus‐Infected Children at 8 Years of Age

1998 ◽  
Vol 178 (4) ◽  
pp. 1019-1023 ◽  
Author(s):  
F. Buseyne ◽  
G. Janvier ◽  
J. P. Teglas ◽  
S. Ivanoff ◽  
M. Burgard ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Chemokine Receptor ◽  
Plasma Virus ◽  
Virus Load ◽  
Immunodeficiency Virus ◽  
Chemokine Receptor Ccr5 ◽  
Plasma Virus Load ◽  
Receptor Ccr5

scholarly journals Relationship between In Vitro Human Immunodeficiency Virus Type 1 Replication Rate and Virus Load in Plasma

2003 ◽  
Vol 77 (22) ◽  
pp. 12105-12112 ◽  
Author(s):  
Thomas B. Campbell ◽  
Kristina Schneider ◽  
Terri Wrin ◽  
Christos J. Petropoulos ◽  
Elizabeth Connick
Keyword(s):  
Replication Capacity ◽  
Replication Rate ◽  
Plasma Virus ◽  
Virus Load ◽  
Immunodeficiency Virus ◽  
Plasma Virus Load ◽  
Hiv 1 ◽  
Rna Concentration

ABSTRACT Although plasma human immunodeficiency virus type 1 (HIV-1) RNA concentration is a major determinant of the rate of HIV-1 disease progression, the reasons for variability in plasma virus loads among infected individuals are not fully understood. We conducted investigations with 15 HIV-1-infected individuals who were not receiving antiretroviral therapy to evaluate the hypothesis that HIV-1 replication rate in vitro is a significant determinant of plasma virus load. Virus could not be isolated from one subject. Two subjects were excluded because they had features previously associated with distinct plasma virus loads and altered rates of disease progression; one harbored a syncytium-inducing virus and the second was heterozygous for a 32-bp deletion from the CCR5 gene. HIV-1 replication rates were determined by culturing autologous virus isolates in phytohemagglutinin-treated peripheral blood mononuclear cells (PBMC) and determining the rate of p24 antigen production during the logarithmic phase of viral replication. The contribution of HIV-1 reverse transcriptase (RT) and protease (PR) alleles to replication capacity was assessed using recombinant viruses in a single-cycle infection assay. HIV-1 replication rates ranged from 0.15 to 0.76 log10 pg/ml/day and were reproducible within the same donor PBMC (coefficient of variation ± 4%). RT-PR replication capacity ranged from 14 to 95% of that of control virus and was linearly related to replication rate (r 2 = 0.53; P = 0.007). Plasma HIV-1 RNA concentration was linearly related to replication rate (r 2 = 0.71; P < 0.001) and RT-PR replication capacity (r 2 = 0.44; P = 0.019). These data suggest that different RT-PR alleles are important determinants of HIV-1 replication rates and that HIV-1 replication rate explains much of the variability in plasma virus load in chronic HIV-1 infection.

scholarly journals A Pathogenic Threshold of Virus Load Defined in Simian Immunodeficiency Virus- or Simian-Human Immunodeficiency Virus-Infected Macaques

1998 ◽  
Vol 72 (12) ◽  
pp. 10281-10285 ◽  
Author(s):  
Peter Ten Haaft ◽  
Babs Verstrepen ◽  
Klaus Überla ◽  
Brigitte Rosenwirth ◽  
Jonathan Heeney
Keyword(s):  
Human Immunodeficiency Virus ◽  
Simian Immunodeficiency Virus ◽  
Rhesus Macaques ◽  
Viral Rna ◽  
Pathogenic Potential ◽  
Virus Load ◽  
Immunodeficiency Virus ◽  
Plasma Virus Load ◽  
Plasma Rna ◽  
Rna Levels

ABSTRACT To determine if a specific pathogenic threshold of plasma viral RNA could be defined irrespective of virus strain, RNA levels in the plasma of more than 50 infected rhesus macaques (Macaca mulatta) were measured. Animals were inoculated intravenously with either simian immunodeficiency virus (SIV) or simian-human immunodeficiency virus (SHIV) strains of known pathogenic potential (SIV8980, SIVsmm-3, SIVmac32H/J5, SIVmac32H/1XC, reverse transcriptase-SHIV, SHIV89.6p) or with attenuated strains (SHIVW6.1D, SHIVsf13, SHIVhan-2, SIVmacΔnef, SHIVsf33). In animals inoculated with nonpathogenic strains, shortly after the primary peak of viremia viral RNA levels declined and remained below 104 RNA equivalents/ml of plasma between 6 and 12 weeks postinoculation. Animals infected with documented pathogenic strains maintained viral RNA levels higher than 105 RNA equivalents/ml of plasma. In animals infected with strains with low virulence, a decline in plasma RNA levels was observed, but with notable individual variation. Our results demonstrate that the disease-causing potential was predicted and determined by a threshold plasma virus load which remained greater than 105 RNA equivalents/ml of plasma 6 to 12 weeks after inoculation. A threshold virus load value which remained below 104 RNA equivalents/ml of plasma was indicative of a nonpathogenic course of infection.

scholarly journals Simian immunodeficiency virus resistance of macaques infused with interferon β-engineered lymphocytes

2000 ◽  
Vol 81 (11) ◽  
pp. 2741-2750 ◽  
Author(s):  
Franck Matheux ◽  
Evelyne Lauret ◽  
Véronique Rousseau ◽  
Jérôme Larghero ◽  
Bertrand Boson ◽  
...  
Keyword(s):  
Simian Immunodeficiency Virus ◽  
Unknown Origin ◽  
Good Health ◽  
Cell Number ◽  
Peripheral Blood Lymphocytes ◽  
Plasma Virus ◽  
Virus Load ◽  
Immunodeficiency Virus ◽  
Plasma Virus Load

To test the in vivo anti-simian immunodeficiency virus (SIV) efficacy of interferon (IFN)-β-engineered lymphocytes, peripheral blood lymphocytes harvested from two uninfected macaques were transduced with a retroviral vector carrying a constitutively expressed IFN-β gene and reinfused, resulting in approximately 1 IFN-β-transduced cell out of 1000 circulating cells. The gene-modified cells were well tolerated and could be detected for at least 74 days without causing any apparent side effects. These two animals together with three untreated control macaques were then infected with SIVmac251. The two IFN-β-infused macaques are in good health, 478 days after infection, with a reduced plasma virus load and sustained numbers of CD4+ and CD8+ cells. Throughout the study, the proportion of IFN-β-transduced cells has been maintained. Of the three control macaques, two were characterized by a high plasma virus load and a decrease in CD4+ cells. One was moribund and was sacrificed 350 days after infection and the other now has fewer than 100 circulating CD4+ cells/ml. Unexpectedly, the third control macaque, which, like the two IFN-β-infused animals, had a low plasma virus load and a maintenance of CD4+ and CD8+ cell number, was characterized by a permanent level of serum IFN-β, of unknown origin, already present before SIV infection. Although no definite conclusion can be made in view of the limited number of animals, these data indicate that further exploration is warranted of an IFN-β-based anti-human immunodeficiency virus gene therapy.

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