Background: Human polyomaviruses (HPyVs) asymptomatically infect the human population during childhood and establish latency in the host. Viral reactivation and urinary excretion can occur when the immune system is impaired. Exposure to particulate air pollution, including the PM10/PM2.5components, is a public health problem and has been linked to several disorders. Studies assessing the relationship between PM10/PM2.5exposure and viral replication are lacking. Objectives: To investigate the relationship between HPyVs viruria and PM10/PM2.5exposures. Methods: Individual environmental exposure was assessed in 50 healthy adult volunteers using a chemical transport model (CTM) with a municipality resolution for daily PM10and monitoring stations data for daily PM2.5exposures. For each subject, a urine sample was collected, and HPyVs (JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and HPyV9) loads were determined. Zero-inflated negative binomial (ZINB) regression was used to model the count data, as it contained excessive zeros. Covariates were chosen by stepwise selection. Results: HPyVs DNA was detected in 54% (median:87.6*105copies/ml) of the urine samples. JCPyV was the prevalent (48%, (median viral load:126*105copies/ml). Considering the load of the most frequently measured HPyVs, JCPyV, in the count-part of the ZINB model, every unitary in PM measured 2 days before urine collection (PM Day −2) was associated with an increase in JCPyV load (PM10: +4.0%, p-value = 0.002; PM2.5: +3.6%, p-value = 0.005). In the zero-part, the significant predictor was the PM10measured 5 days before urine collection (+3%, p-value = 0.03). Conclusions: The environmental levels of PM10/PM2.5increase the JCPyV viruria. Our findings emphasize the need for studies assessing the influence of air pollution exposure on the risk of viral reactivation. The environmental levels of PM10/PM2.5increase the Human JC Polyomavirus viruria, showing an increasing risk of viral replication linked to the air pollution exposure.
Particulate matter exposure increases JC polyomavirus replication in the human host
Cattaneo, Andrea;
2018-01-01
Abstract
Background: Human polyomaviruses (HPyVs) asymptomatically infect the human population during childhood and establish latency in the host. Viral reactivation and urinary excretion can occur when the immune system is impaired. Exposure to particulate air pollution, including the PM10/PM2.5components, is a public health problem and has been linked to several disorders. Studies assessing the relationship between PM10/PM2.5exposure and viral replication are lacking. Objectives: To investigate the relationship between HPyVs viruria and PM10/PM2.5exposures. Methods: Individual environmental exposure was assessed in 50 healthy adult volunteers using a chemical transport model (CTM) with a municipality resolution for daily PM10and monitoring stations data for daily PM2.5exposures. For each subject, a urine sample was collected, and HPyVs (JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and HPyV9) loads were determined. Zero-inflated negative binomial (ZINB) regression was used to model the count data, as it contained excessive zeros. Covariates were chosen by stepwise selection. Results: HPyVs DNA was detected in 54% (median:87.6*105copies/ml) of the urine samples. JCPyV was the prevalent (48%, (median viral load:126*105copies/ml). Considering the load of the most frequently measured HPyVs, JCPyV, in the count-part of the ZINB model, every unitary in PM measured 2 days before urine collection (PM Day −2) was associated with an increase in JCPyV load (PM10: +4.0%, p-value = 0.002; PM2.5: +3.6%, p-value = 0.005). In the zero-part, the significant predictor was the PM10measured 5 days before urine collection (+3%, p-value = 0.03). Conclusions: The environmental levels of PM10/PM2.5increase the JCPyV viruria. Our findings emphasize the need for studies assessing the influence of air pollution exposure on the risk of viral reactivation. The environmental levels of PM10/PM2.5increase the Human JC Polyomavirus viruria, showing an increasing risk of viral replication linked to the air pollution exposure.
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