Diagnostic value of human cytomegalovirus DNA PCR regarding different clinical specimens

1996 ◽  
Vol 52 (4) ◽  
pp. 304-305
Author(s):  
S. Prösch ◽  
H. Meisel ◽  
E. Schielke ◽  
K. M. Einhäupl ◽  
D. H. Krüger
1984 ◽  
Vol 150 (1) ◽  
pp. 121-126 ◽  
Author(s):  
S. A. Spector ◽  
J. A. Rua ◽  
D. H. Spector ◽  
R. McMillan

2019 ◽  
Vol 51 (2) ◽  
pp. 51-58 ◽  
Author(s):  
Yun-yan Lou ◽  
Qiong-dan Wang ◽  
Yu-tian Lu ◽  
Meng-yun Tu ◽  
Xi Xu ◽  
...  

Human cytomegalovirus (HCMV) is an opportunistic prototypic beta-herpesvirus that can cause severe and even fatal diseases in immune-naive newborns and immunocompromised adults. Host-virus interactions occurring at the transcriptional and posttranscriptional levels are critical for establishing an HCMV latent or lytic infection, but the mechanisms remain poorly understood. Herein, we investigated the expression of circRNAs in human leukemia monocytes (THP-1 cells) latently infected with HCMV and explored the diagnostic value of circRNAs in children with HCMV infection. A total of 2,110 and 1,912 circRNAs were identified in mock-infected and HCMV latent-infected THP-1 cells, respectively. Of these, we identified 1,421 differently expressed circRNAs, of which 650 were upregulated and 771 were downregulated. The host genes corresponding to the differentially expressed circRNAs were mainly involved in the regulation of host cell secretion pathways, cell cycle, and cell apoptosis. The differentially expressed circRNAs had binding sites for microRNAs, suggesting an important role in the mechanism of HCMV latent infection. Furthermore, a clinical analysis showed that the expression levels of hsa_circ_0001445 and hsa_circ_0001206 were statistically significantly different in HCMV-infected patients vs. normal controls, suggesting that these circRNAs could potentially serve as biomarkers of HCMV-infection.


2021 ◽  
Vol 09 (02) ◽  
pp. 110-116
Author(s):  
Weijia Lin ◽  
Zhi Liu ◽  
Yaping Zhang ◽  
Feng Li ◽  
Xiulong Zhang ◽  
...  
Keyword(s):  

1995 ◽  
Vol 21 (Supplement_2) ◽  
pp. S170-S173 ◽  
Author(s):  
Stephen A. Spector ◽  
Karen Usia ◽  
Dana Wolf ◽  
Mika Shinkai ◽  
Irene Smith

2013 ◽  
Vol 57 (5) ◽  
pp. 396-399 ◽  
Author(s):  
Tohru Daikoku ◽  
Kazuhide Saito ◽  
Takamitsu Aihara ◽  
Masahiro Ikeda ◽  
Yoshiyuki Takahashi ◽  
...  

2021 ◽  
Vol 09 (03) ◽  
pp. 124-130
Author(s):  
Weijia Lin ◽  
Zhi Liu ◽  
Yaping Zhang ◽  
Yanan Yu ◽  
Yang Liu ◽  
...  

2019 ◽  
Vol 93 (17) ◽  
Author(s):  
Rebecca M. Brown ◽  
Pranav S. J. B. Rana ◽  
Hannah K. Jaeger ◽  
John M. O’Dowd ◽  
Onesmo B. Balemba ◽  
...  

ABSTRACTCongenital human cytomegalovirus (HCMV) infection causes a broad spectrum of central and peripheral nervous system disorders, ranging from microcephaly to hearing loss. These ramifications mandate the study of virus-host interactions in neural cells. Neural progenitor cells are permissive for lytic infection. We infected two induced pluripotent stem cell (iPSC) lines and found these more primitive cells to be susceptible to infection but not permissive. Differentiation of infected iPSCs inducedde novoexpression of viral antigens. iPSCs can be cultured in three dimensions to generate cerebral organoids, closely mimickingin vivodevelopment. Mock- or HCMV-infected iPSCs were subjected to a cerebral organoid generation protocol. HCMV IE1 protein was detected in virus-infected organoids at 52 days postinfection. Absent a significant effect on organoid size, infection induced regions of necrosis and the presence of large vacuoles and cysts. Perhaps more in parallel with the subtler manifestations of HCMV-induced birth defects, infection dramatically altered neurological development of organoids, decreasing the number of developing and fully formed cortical structure sites, with associated changes in the architectural organization and depth of lamination within these structures, and manifesting aberrant expression of the neural marker β-tubulin III. Our observations parallel published descriptions of infected clinical samples, which often contain only sparse antigen-positive foci yet display areas of focal necrosis and cellular loss, delayed maturation, and abnormal cortical lamination. The parallels between pathologies present in clinical specimens and the highly tractable three-dimensional (3D) organoid system demonstrate the utility of this system in modeling host-virus interactions and HCMV-induced birth defects.IMPORTANCEHuman cytomegalovirus (HCMV) is a leading cause of central nervous system birth defects, ranging from microcephaly to hearing impairment. Recent literature has provided descriptions of delayed and abnormal maturation of developing cortical tissue in infected clinical specimens. We have found that infected induced pluripotent stem cells can be differentiated into three-dimensional, viral protein-expressing cerebral organoids. Virus-infected organoids displayed dramatic alterations in development compared to those of mock-infected controls. Development in these organoids closely paralleled observations in HCMV-infected clinical samples. Infection induced regions of necrosis, the presence of larger vacuoles and cysts, changes in the architectural organization of cortical structures, aberrant expression of the neural marker β-tubulin III, and an overall reduction in numbers of cortical structure sites. We found clear parallels between the pathologies of clinical specimens and virus-infected organoids, demonstrating the utility of this highly tractable system for future investigations of HCMV-induced birth defects.


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