Powassan/Deer Tick Virus and Borrelia Burgdorferi Infection in Wisconsin Tick Populations.

Powassan/Deer Tick Virus (POWV/DTV) is an emerging cause of arboviral neuroinvasive disease in the upper Midwest. These studies describe the prevalence and geographic distribution of Wisconsin ticks carrying POWV/DTV as well as the high frequency of Ixodes scapularis ticks coinfected with both POWV/DTV and Borrelia burgdorferi, the causative agent of Lyme disease. These findings suggest that concurrent transmission of POWV/DTV and B.

No evidence of murine-like gammaretroviruses in CFS patients previously identified as XMRV-infected.

Members of the gammaretroviruses--such as murine leukemia viruses (MLVs), most notably XMRV [xenotropic murine leukemia virus (X-MLV)-related virus--have been reported to be present in the blood of patients with chronic fatigue syndrome (CFS). We evaluated blood samples from 61 patients with CFS from a single clinical practice, 43 of whom had previously been identified as XMRV-positive. Our analysis included polymerase chain reaction and reverse transcription polymerase chain reaction procedures for detection of viral nucleic acids and assays for detection of infectious virus and virus-specific antibodies.

TNF-alpha inhibits insulin action in liver and adipose tissue: A model of metabolic syndrome.

Several studies suggest that TNF-alpha contributes to the development of insulin resistance (IR). We compared transcriptional profiles of rat H-411E liver cells exposed to insulin in the absence or presence of TNF-alpha. We identified 33 genes whose expression was altered by insulin, and then reversed by TNF-alpha.

Susceptibility to severe Streptococcal sepsis: use of a large set of isogenic mouse lines to study genetic and environmental factors.

Variation in responses to pathogens is influenced by exposure history, environment and the host's genetic status. We recently demonstrated that human leukocyte antigen class II allelic differences are a major determinant of the severity of invasive group A streptococcal (GAS) sepsis in humans. While in-depth controlled molecular studies on populations of genetically well-characterized humans are not feasible, it is now possible to exploit genetically diverse panels of recombinant inbred BXD mice to define genetic and environmental risk factors.

Role of nuclear factor-kappaB in the antiviral action of interferon and interferon-regulated gene expression.

Interferons (IFNs) play critical roles in host defense by modulating the expression of various genes via tyrosine phosphorylation of STAT transcription factors. IFN-alpha/beta activates another important transcription factor, nuclear factor-kappaB (NF-kappaB), but its role in IFN-mediated activity is poorly understood. Sensitivity to the antiviral and gene-inducing effects of IFN was examined in normal fibroblasts and in NF-kappaB knockout fibroblasts from p50- and p65-null mice.

Persistent lack of human herpesvirus-6 specific T-helper cell response in liver transplant recipients.

Background: Specific immunologic defects predisposing to human herpesvirus-6 (HHV-6), e.g. the role of HHV-6 specific T-helper cell memory response in liver transplant recipients, have not been assessed.

Human herpesvirus 6 infection mimicking juvenile myelomonocytic leukemia in an infant.

In vitro cell culture studies of bone marrow and peripheral blood progenitor cells from patients with juvenile myclomonocytic leukemia (JMML) consistently show spontaneous proliferation and selective hypersensitivity to granulocyte-macrophage colony-stimulating factor (GM-CSF). This GM-CSF hypersensitivity dose-response assay has become a component of the international diagnostic criteria for JMML. The authors report a 2-week-old boy with perinatal human herpesvirus 6 (HHV-6) infection in whom in vitro bone marrow culture studies suggested the diagnosis of JMML by showing increased spontaneous proliferation, inhibition of this growth by anti-GM-CSF antibodies, and hypersensitivity to GM-CSF.

Impact of human herpesvirus-6 on the frequency and severity of recurrent hepatitis C virus hepatitis in liver transplant recipients.

A role of tumor necrosis factor-alpha (TNF-alpha) In the immunopathogenesis of hepatitis C virus (HCV) infection has been proposed. The novel herpes virus, human herpes virus-6 (HHV-6), is amongst the most potent inducers of cytokines, including TNF-alpha. The impact of HHV-6 viremia on the progression of recurrent HCV hepatitis was assessed in 51 HCV-positive liver transplant recipients.

Human herpesvirus 6: diagnosis of active infection.

HHV-6 is an opportunistic viral pathogen that has been demonstrated as the cause of often life-threatening illness in pediatric patients and transplant recipients. A substantial body of scientific evidence links HHV-6 to the etiology of such chronic diseases as multiple sclerosis. For these reasons, it is important that patients in these groups be screened for possible infection with HHV-6.

Human herpesvirus 6 and multiple sclerosis: systemic active infections in patients with early disease.

By means of immunohistochemical staining, cells actively infected with human herpesvirus 6 (HHV-6) were found in central nervous system tissues from 8 (73%) of 11 patients with definite multiple sclerosis (MS). Interestingly, 17 (90%) of 19 tissue sections showing active demyelination were positive for HHV-6-infected cells compared with only 3 (13%) of 23 tissue sections free of active disease (P<.0001).

Human herpesvirus-6 in liver transplant recipients: role in pathogenesis of fungal infections, neurologic complications, and outcome.

Background: The clinical impact and relevance of human herpesvirus-6 (HHV-6) infection in liver transplant recipients, has not been fully discerned.

Methods: A prospective study of 80 consecutive liver transplant recipients was performed using surveillance cultures for HHV-6 at weeks 2, 3, 4, and 6 after transplantation. Viral isolation was used for the detection of HHV-6.

Encephalopathy associated with human herpesvirus 6 in a liver transplant recipient.

Recent reports have documented human herpesvirus 6 (HHV-6) as a cause of high fever, bone marrow depression, and rash in liver transplant recipients in the absence of another known pathogen. We describe a 49-year-old liver transplant recipient who developed confusion, occipital headache, and involuntary movements of the limbs 3 weeks after orthotopic liver transplantation. HHV-6 was detected in the peripheral blood using a rapid culture assay.

Counselor prompts to increase condom taking during treatment for cocaine dependence.

This study examined whether active prompting would increase the number of free condoms taken from dispensers placed in counselors' offices in a cocaine abuse treatment clinic. Using a combined multiple baseline and reversal design, two teams of counselors were instructed to actively prompt and encourage condom taking during some conditions and to avoid commenting on or encouraging condom use in other conditions. To monitor accuracy of implementing the intervention, counselors completed a checklist for every subject they saw in their office during the day.

Human herpesvirus-6 infection in liver transplant recipients: documentation of pathogenicity.

Background: The new herpesvirus, human herpesvirus-6 (HHV-6), is able to cause clinical illness after transplantation; however, the pathogenic potential and the clinical features of HHV-6 have not been defined in liver transplant recipients.

Methods: We report the first cases of invasive and symptomatic infection due to HHV-6 in liver transplant recipients.

Results: HHV-6 infection occurred in four liver transplant recipients at a median of 50 days after transplant (range 17-90 days).

Adenovirus infections in immunocompromised patients.

Adenovirus infections have been reported in as many as one-fifth of bone marrow transplant (BMT) recipients and patients with acquired immunodeficiency syndrome (AIDS), and in a lesser, though still prominent, proportion of organ transplant recipients. The relative contributions of primary infections versus reactivations from latency in immunocompromised patients remain unclear. Compared with adult BMT recipients, pediatric BMT recipients appear to be infected by adenovirus more frequently and earlier in the post-transplant period.

Prevalence of human herpesvirus 6 in lung tissue from children with pneumonitis.

Aims/background: Human herpesvirus type 6 (HHV-6) is the aetiological agent of exanthem subitum, and has also been linked with a variety of other diseases. The aim of this study was to investigate the role of HHV-6 in pneumonitis in children.

Methods: Formalin fixed, paraffin wax embedded lung tissue from 33 children (age range two months to 16 years) who died with pneumonitis was subjected to immunohistochemical staining for HHV-6 using an avidin-biotin method.

Plasmodium falciparum merozoite adhesion is mediated by sialic acid.

The invasion of host red blood cells by Plasmodium falciparum merozoites is a complex process requiring multiple receptor-ligand interactions. Glycophorin A, a sialic acid-rich integral membrane protein, is an important RBC receptor for merozoites. We stably expressed glycophorin A in wild type Chinese hamster ovary (CHO) cells and in Lec 2 CHO cells which have a defect in the ability to sialylate proteins.

Subacute leukoencephalitis caused by CNS infection with human herpesvirus-6 manifesting as acute multiple sclerosis.

Several recent reports have documented the neuroinvasiveness of human herpesvirus-6 (HHV-6) in infants with primary HHV-6 infections, in children and adults with AIDS, in recipients of bone marrow transplants, and in immunologically intact adults and children. CNS infections with HHV-6 can be subacute and are frequently associated with diffuse or multifocal demyelination. We analyzed the CNS tissues of a young woman who died of a demyelinative disease, which was clinically and histopathologically diagnosed as acute multiple sclerosis, for active HHV-6 infection by immunohistochemical staining.

Human herpesvirus-6 in transplantation: an emerging pathogen.

Background: Human herpesvirus-6 can be an opportunistic pathogen in transplant recipients.

Purpose: To summarize the epidemiologic and clinical aspects of human herpesvirus-6 infection, the immunologic basis of the pathogenicity of human herpesvirus-6, and the management of human herpesvirus-6 infection in transplant recipients.

Data Sources: English-language articles identified through a MEDLINE search from 1986 (when human herpesvirus-6 was discovered) to the present, bibliographies of identified articles, and recognized texts.

Active HHV-6 infection in the lymph nodes of HIV-infected patients: in vitro evidence that HHV-6 can break HIV latency.

Studies published previously by this laboratory have demonstrated that patients with AIDS have widely disseminated, active infections with HHV-6 at the time of their death. However, it remains unclear when in the course of the human immunodeficiency virus (HIV) infection the active HHV-6 infection first appears. To address this question, lymph node biopsies from 10 HIV-infected patients were analyzed for active human herpesvirus 6 (HHV-6) infections by immunohistochemical staining.

Variant B human herpesvirus-6 associated febrile dermatosis with thrombocytopenia and encephalopathy in a liver transplant recipient.

Human herpesvirus 6 (HHV-6) is a recently discovered virus the pathogenicity of which in solid organ transplant recipients has not been defined. We describe a unique febrile syndrome due to disseminated invasive variant B HHV-6 infection in a liver transplant recipient with evidence of direct tissue invasion by the virus. Acute febrile illness characterized by life-threatening thrombocytopenia, progressive encephalopathy and skin rash developed in association with invasive HHV-6 infection in a liver transplant recipient.

Chronic myelopathy associated with human herpesvirus-6.

Human herpesvirus-6 (HHV-6) is implicated in a variety of neurologic diseases. We report a previously healthy elderly woman with progressive spastic paraparesis. At autopsy the spinal cord showed widespread demyelination, axonal loss, and chronic inflammation.