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The evidence demonstrates that the immune system centrally determines disease outcome in both cases.
This analysis also illustrates how complex biochemical signals can be translated into cell fitness that determines disease dynamics.
During early HIV-1 infection (EHI), the interaction between the immune response and the virus determines disease progression.
The previously developed MWS-DAS determines disease activity in nine MWS domains attributing 0, 1, or 2 points to each level of disease activity [ 32].
Numerous cytokines, both proinflammatory and anti-inflammatory, have been detected in RA patients, and the balance between the activities of these opposing cytokines determines disease severity [ 4].
Therefore, for both diseases, at least in mouse models, the genotype of bone marrow-derived cells determines disease development, and not that of the host.
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Prior imaging genetics research typically employs a two-step procedure for identifying risk factors and biomarkers: one first determines disease-relevant QTs, and then detects the biomarkers associated with these QTs.
It was an investigation of epigenetics, a popular area of molecular biology that looks for modifications of genes that can help determine disease risk.
Genetic differences may determine disease predisposition and therapeutic response in some diseases.
HHV-6 DNA integration may lead to difficulties in disease diagnosis and determining disease resolution.
Defects or aberrancy of this protective response pathway may determine disease susceptibility during ambient particle exposure.
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