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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Viral Load

 
 
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Disease relevance of Viral Load

  • We present data from that trial showing the number of infected infants at 18 months of age and the relation between the maternal viral load, the risk of HIV-1 transmission, and the efficacy of zidovudine treatment [1].
  • These experiments are the first to demonstrate that a human class II DR gene can alter the severity of demyelination in an animal model of MS without influencing viral load [2].
  • METHODS: One hundred forty-one patients who previously did not respond to IFN and ribavirin, 86% with genotype 1 or 4 infection, 52% with high viral load (>800.000 IU/mL), 22% with cirrhosis, were retreated with pegylated IFN-alpha-2b 1.5 microg/kg per week and ribavirin 1000-1200 mg/day for 48 weeks and followed up for 24 weeks [3].
  • However, unlike that in HAM/TSP patients, the viral load in peripheral-blood mononuclear cells was not necessarily high in the seropositive Sjögren syndrome group [4].
  • MEASUREMENTS: Change in size of the parotid cyst, CD4 lymphocyte count, and HIV viral load [5].
 

Psychiatry related information on Viral Load

  • OBJECTIVE: To describe the cost and outcome associated with the use of CD4 cell count and viral load tests as part of screening strategies to identify persons eligible for subsidized antiretroviral therapy (ART) in Côte d'Ivoire [6].
  • Furthermore, CD4 count and CSF viral load, but not plasma viral load, showed significant effects on cerebral metabolite concentrations, which in turn showed significant effects on the HIV-dementia scale [7].
  • After recurrence of PTSD, the patient showed an important decrease in viral load and a higher CD4 level despite a bad compliance to antiretrovirals [8].
  • Factors associated with final viral load < 50 copies/ml included not being a cigarette smoker, receiving lamivudine in one's final regimen, and having an HIV risk behavior other than male-male sex [9].
  • After adjusting for education, race, substance dependence, antiretroviral medication status, viral load, CD4 lymphocyte count, and Beck Depression Inventory score, the odds of having HAD among individuals in the older group was 3.26 (1.32 to 8.07) times that of the younger group [10].
 

High impact information on Viral Load

  • Remarkably, blocking the interaction between PD-1 and its ligand, PD-L1, reactivates these T cells and reduces viral load [11].
  • The high viral burden in mononuclear cells was confirmed by quantitative studies using a polymerase-chain-reaction method [12].
  • Tlr3-deficient (Tlr3(-/-)) mice were more resistant to lethal WNV infection and had impaired cytokine production and enhanced viral load in the periphery, whereas in the brain, viral load, inflammatory responses and neuropathology were reduced compared to wild-type mice [13].
  • Although subjects with CCR5 delta 32 defects had significantly reduced median viral load at study entry, providing a plausible explanation for the association with delayed progression, this association was not seen with CCR2B 64I [14].
  • The estimated infected cell death rate exhibited large interpatient variation (corresponding t1/2 = 1.7 to 70 days), was inversely correlated with baseline viral load, and was positively correlated with alanine aminotransferase levels [15].
 

Chemical compound and disease context of Viral Load

 

Biological context of Viral Load

 

Anatomical context of Viral Load

  • Using an anti-p27(CA) MMTV antibody, viral proteins were detected in the perihepatic lymph nodes but not in liver tissue samples from patients with PBC, suggesting a higher viral burden in lymphoid tissue [26].
  • HIV-infected subjects with undetectable viral load recovered mature CD3(-)/CD161(+)/CD56(+) NK cells and cytotoxicity against tumor (K562) and HSV-infected target cells to percentages comparable with those of uninfected individuals, but their NK cells remained impaired in their ability to produce IFN-gamma [27].
  • METHODS: Twelve HIV-1-infected men on NVP-containing regimens including 3TC (n = 8) or D4T (n = 11) provided 23 blood plasma and 22 seminal plasma samples for drug concentration and viral load quantitation [28].
  • These findings support current approaches to the identification of HIV-specific CD8 T lymphocyte reactivity based on leukocytes isolated from blood even in patients with ART-induced suppression of viral load [29].
  • These results indicate that in the late stage of disease with increasing viral load and diversity, CCR5 utilization and M-tropism persist in blood and tissue and the replicative ability in macrophages increases [30].
 

Associations of Viral Load with chemical compounds

  • CONCLUSIONS: Triple drug therapy with zidovudine, didanosine, and nevirapine led to a substantially greater and sustained decrease in plasma viral load than the 2-drug regimens studied [31].
  • MAIN OUTCOME MEASURES: At virologic failure (S1 sample) and 6 weeks later (S2 sample), assessment of protease and reverse transcriptase gene mutations, plasma indinavir level, and degree of viral load rebound; pill count during induction and maintenance periods [32].
  • The proportions of patients with a viral load below 200 copies/mL in the saquinavir, indinavir, nelfinavir, and placebo arms were 34% (40/116), 36% (25/69), 34% (47/139), and 23% (36/157), respectively [33].
  • RESULTS: Ribavirin monotherapy induced a significant, moderate, early, and transient viral load decrease in approximately half of the patients [34].
  • There was no association with viral load, sex, type of interferon, or cholesterol levels [35].
 

Gene context of Viral Load

  • DRB1 and DQB1 alleles did not influence viral load as an independent factor [36].
  • IL-12p70, IL-4 and tumour necrosis factor-alpha concentrations were consistently highest within 5 days of peak viral load [37].
  • Dysregulation of membrane-bound tumor necrosis factor-alpha and tumor necrosis factor receptors on mononuclear cells in human immunodeficiency virus type 1 infection: low percentage of p75-tumor necrosis factor receptor positive cells in patients with advanced disease and high viral load [38].
  • Expression levels for IL-10, IFN-gamma and CXCL10 consistently peaked within 4 days of peak viral load [37].
  • The STAT1 pathway is necessary for clearing the initial viral load, whereas the STAT1-independent pathway controls later viral burden and prevents DEN disease in mice [39].
 

Analytical, diagnostic and therapeutic context of Viral Load

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  23. Sequential involvement of Cdk1, mTOR and p53 in apoptosis induced by the HIV-1 envelope. Castedo, M., Roumier, T., Blanco, J., Ferri, K.F., Barretina, J., Tintignac, L.A., Andreau, K., Perfettini, J.L., Amendola, A., Nardacci, R., Leduc, P., Ingber, D.E., Druillennec, S., Roques, B., Leibovitch, S.A., Vilella-Bach, M., Chen, J., Este, J.A., Modjtahedi, N., Piacentini, M., Kroemer, G. EMBO J. (2002) [Pubmed]
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