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Human cytomegalovirus DNA level in patients with idiopathic pulmonary fibrosis

84%
The objectives of the study were to estimate human cytomegalovirus (HCMV) DNA copy number in broncho-alveolar lavage cells, blood leukocytes, and serum of patients with idiopathic pulmonary fibrosis (IPF). The study groups consisted of 16 patients, newly diagnosed with IPF and never treated, (mean age 40.9 ±11.0 yr; F/M-7/9) and in 16 adult healthy volunteers (mean age 36.8 ±6.4 yr; F/M-4/12) used as controls. The HCMV DNA copy number was calculated by a Q-PCR method using TaqMan ABI PRISMTM7700. We found that the prevalence of the HCMV DNA positive subjects in the patient group (75%) did not differ significantly from that in the control group (69%). We also found that in both patient and control groups the mean HCMV DNA copy number in BAL cells was significantly higher than that in blood leukocytes (log10=2.7 vs. 1.2 for patients and 2.8 vs. 0.9 for controls, respectively). However, a higher HCMV DNA copy number in blood serum was observed in IPF patients than in controls (log10=3.2 vs. 2.0, respectively). We conclude that the lungs play an important role in the human pathobiology of cytomegalovirus sustenance.
Oxidative stress, i.e., excessive production of oxygen free radicals and reactive oxygen species, leads to lipid peroxidation and to formation of reactive aldehydes which act as second messengers of free radicals. It has previously been shown that oxidative stress may be involved in the transcriptional regulation of cytomegalovirus (CMV) immediate early promoter, involved in viral reactivation from latency. In the current study we used a plasmid containing the yellow fluorescent protein (YFP) gene under the control of CMV-1 promoter to monitor the influence of hydrogen peroxide and reactive aldehydes, 4-hydroxy-2-nonenal (HNE) and acrolein, on CMV-1 promoter activation in human embryonic kidney cells (HEK293). While acrolein was ineffective, hydrogen peroxide slightly (50 %) stimulated the CMV promoter. In contrast, HNE had a strong, up to 3-fold, enhancing effect on the CMV-1 promoter within four as well as after 24 h of treatment. The most effective was the treatment with 24 μM HNE. This effect of HNE suggests that stressful conditions associated with lipid peroxidation could lead to CMV activation.
The cytomegalovirus (CMV) genome encodes four clusters of genes expressed immediately after infection — i.e.: UL36-38, UL122-123, TRS1-IRS1, and US3. The general function of these genes is associated with inhibition of cellular mechanisms of antiviral response. Although several biological processes have been mapped onto specific gene products, the knowledge of the molecular mechanism of their activity remains fragmentary. Here, we report the application of protein structure prediction methods in assigning the function to a glycosylated domain encoded by UL37 of CMV (gpUL37, UL37x3). The discerned similarity clearly points out that this domain represents a novel type of a major histocompatibility complex (MHC)-like protein, and consequently may play a central role in an additional mechanism of escape from antiviral response.
It has been suggested that some microorganisms may play a role in the etiology or progression of atherosclerotic plaques. The purpose of this study was to assess for the presence of Helicobacter pylori and cytomegalovirus (CMV) DNA using polymerase chain reaction (PCR) technique in vascular-wall specimens obtained during autopsy. Four to 5 mm long samples from 3 different vascular wall specimens (coronary, carotid and abdominal aortas) of 30 patients (23 male, 7 female) were taken for pathologic and microbiologic investigations during autopsy. H. pylori DNA was found in 48.2% atherosclerotic and 19.6% non-atherosclerotic vascular wall specimens, whereas CMV DNA was found in 37.9% atherosclerotic and 32.7% non-atherosclerotic vascular wall specimens. In terms of CMV DNA detection, no statistically significant differences between the atherosclerotic and non-atherosclerotic groups were present (P>0.05). However, there was a statistically significant difference between the atherosclerosis and non-atherosclerotic groups in terms of H. pylori DNA in coronary and abdominal aorta arteries (p = 0.016 and p = 0.0029 respectively) but not in carotid arteries (p= 1.00). In conclusion, the correlation between H. pylori and atherosclerosis could be suggested. These finding warrant further investigation regarding the role of H. pylori in atherosclerosis.
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