Objective: We examined the frequency and characteristics of chromosomally integrated human herpesvirus 6 among congenitally infected children.
Methods: Infants with and without congenital human herpesvirus 6 infection were prospectively monitored. Cord blood mononuclear cell, peripheral blood mononuclear cell, saliva, urine, and hair follicle samples were examined for human herpesvirus 6 DNA. Human herpesvirus 6 RNA, serum antibody, and chromosomally integrated human herpesvirus 6 levels were also assessed.
Results: Among 85 infants, 43 had congenital infections and 42 had postnatal infections. Most congenital infections (86%) resulted from chromosomally integrated human herpesvirus 6; 6 infants (14%) had transplacental infections. Children with chromosomally integrated human herpesvirus 6 had high viral loads in all sites (mean: 5-6 log(10) genomic copies per mug of cellular DNA); among children with transplacental infection or postnatal infection, human herpesvirus 6 DNA was absent in hair samples and inconsistent in other samples, and viral loads were significantly lower. One parent of each child with chromosomally integrated human herpesvirus 6 who had parental hair samples tested had hair containing human herpesvirus 6 DNA. Variant A caused 32% of chromosomally integrated human herpesvirus 6 infections, compared with 2% of postnatal infections. Replicating human herpesvirus 6 was detected only among chromosomally integrated human herpesvirus 6 samples (8% of cord blood mononuclear cells and peripheral blood mononuclear cells). Cord blood human herpesvirus 6 antibody levels were similar among children with chromosomally integrated human herpesvirus 6, transplacental infection, and postnatal infection and between children with maternal and paternal chromosomally integrated human herpesvirus 6 transmission.
Conclusions: Human herpesvirus 6 congenital infection results primarily from chromosomally integrated virus which is passed through the germ-line. Infants with chromosomally integrated human herpesvirus 6 had high viral loads in all specimens, produced human herpesvirus 6 antibody, and mRNA. The clinical relevance needs study as 1 of 116 newborns may have chromosomally integrated human herpesvirus 6 blood specimens.
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http://dx.doi.org/10.1542/peds.2007-2838 | DOI Listing |
Am J Dermatopathol
January 2025
Department of Dermatology, Columbia University Medical Center, New York, NY; and.
Primary effusion lymphoma (PEL) is a rare and aggressive B-cell lymphoma typically associated with human herpesvirus 8 (HHV-8) and Epstein-Barr virus infections. It classically presents as a malignant effusion in body cavities, but rarely presents with an extracavitary variant characterized by solid tumors in lymph nodes or extranodal sites such as the gastrointestinal tract, skin, lungs, and nervous system. This case report describes an unusual presentation of primary cutaneous extracavitary PEL in an HIV-positive patient that has only been reported in 8 cases previously.
View Article and Find Full Text PDFCancer Immunol Immunother
January 2025
Department of Dermatology and National Center for Tumor Diseases (NCT), Medical Faculty Heidelberg, NCT Heidelberg, a partnership between DKFZ and University Hospital Heidelberg, Heidelberg University, Heidelberg, Germany.
Cytomegalovirus (CMV) infection or reactivation in immune-compromised individuals can lead to a wide range of severe complications including hepatitis. However, its relation with immune checkpoint inhibitors (ICIs) induced hepatitis (ICI-hepatitis) and tumor responses in advanced melanoma patients remains unclear. Hundred and ninety metastatic cutaneous melanoma patients (mCM) who received ICI treatment, with CMV IgG or IgM information available at baseline, were included in the study (Cohort 1).
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Nottingham University Hospitals NHS Trust, Nottingham, United Kingdom.
Background: Early Onset Alzheimer's Disease (EOAD) is thought to result from a combination of environmental, genetic, and lifestyle factors. Herpesvirus infections may contribute to the development of EOAD and the objective of our study is to identify potential associations between herpes virus infections and the risk of developing EOAD.
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Background: Millions of people suffer from traumatic brain injury (TBI) annually and many subsequently develop AD-like characteristics, but the processes occurring in the brain and the reasons for the acquisition of AD-like dementia are unknown. TBI is the leading cause of mortality in young adults and causes a huge socioeconomic burden. Improving outcomes in these patients would be a significant public health benefit.
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