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Both HHV-6A and B are found throughout the brain but HHV-6A appears to have greater potential for central nervous system damage. Several lab studies indicate HHV-6A is more effective at producing (re-)productive infections in immune and central nervous system (CNS) cells. HHV-6B is the strain most commonly reactivated during organ and stem cell transplantation and is also increased in virally derived encephalitic (central nervous system) conditions (Dewhurst 2004). After the initial infection both HHV6A and B can persist in a latent state or in a state of chronic low-level replication for decades. In vitro tests indicate HHV-6 can infect many different cell types including dendritic cells, NK cells and fibroblasts as well as liver, epithelial and endothelial cells and the glial cells in the brain (astrocytes, oligodendrocytes, microglia). Although HHV-6 is able to infect many cells, in only a few is it able to progress to the ‘lytic phase’. In even the most productive infections, however, viral yields are low compared to other infections (Campadelli-Fiume et al.
Several of the serious effects of HHV-6 infection are associated with the immunosuppression that occurs during organ transplantation (Campadelli-Fiume et al. HHV-6 may be a co-factor in a wide array of immunological disorders including infectious mononucleosis, hepatitis, multiple sclerosis, meningoencephalitis and pneumonitis (Flammond et al.
The idea that HHV-6 is able to catalyze HIV activity and patients’ progression to AIDS was proposed early in the AIDS epidemic. Epidemiological studies have not thus far, however, indicated that HHV-6 infection speeds the progression of AIDS. In vitro studies indicate that HHV-6 infection of B-cells triggers the production of a nuclear protein (called Zebra) that turns on genes which are active early in the life cycle of the Epstein-Barr herpesvirus (EBV).
PCR evidence of HHV-6 infection was found in approximately 2% of patients hospitalized with symptoms of encephalitis or meningitis.
The strongest evidence of HHV-6’s potential to cause central nervous damage concerns HHV-6A and multiple sclerosis. The detection of HHV-6 antigens in the oligodendrocytes, astrocytes, microglia and neurons in patients with MS and HHV-6 encephalopathy indicates HHV-6 reactivation may be associated with these diseases (Yoshikawa and Asano 2000).
Both oligodendrocytes and astrocytes originate from cells called glial precursor cells (GPCs) that appear to be underactive in demyelinating diseases such as MS.
HHV-6 also appears to tilt the production of a kind of oligodendrocyte that is particularly vulnerable to TNF-a, a pro-inflammatory cytokine found in MS lesions (Dietrich et al.
While most researchers have been concerned with HHV-6’s effects on the CNS, recent studies suggest several ways HHV-6 is able to alter immune functioning. Simply by binding to the CD 46 receptor HHV-6A appears able to down-regulate it possibly increasing the risk of tissue damage during immune activation. HHV-6A infection of the endothelial cells lining the blood vessels could cause a central nervous system vasculitis. Lerner AM, Beqaj SH, Deeter RG, Dworkin HJ, Zervos M, Chang CH, Fitzgerald JT, Goldstein J, O’Neill W. The material on this site has been compiled by laypeople and Phoenix Rising does not guarantee the accuracy or completeness of the content. Mayo Clinic Channel – YouTubeMedical Edge Mayo Clinic Medical Edge is a weekly medical news insert for television newscasts. The Updated Herpes Handbook(CMV), varicella-zoster virus (VZV), Epstein–Barr virus (EBV), human herpes virus 6 (HHV 6), human a while to see how well one can predict a recurrence. Acute And Recurrent Viral Meningitis(with each recurrence due to a different serotype), repeated Epstein–Barr virus Mainly in immunosuppressed persons siently improved symptoms but often fail to clear the virus from the CSF.
PATIENT INFORMATION ON VALCYTE TREATMENT FOR CHRONIC FATIGUE …PATIENT INFORMATION ON VALCYTE TREATMENT . Protein In Virus Linked To Chronic Fatigue SyndromeObviously, it's great to know this virus is there and that Valcyte helps fight it. Human herpesvirus 7: Closely related to HHV-6, human herpesvirus 7 has also been linked to roseola.
Increasing evidence suggests, however, that not only does HHV-6A vary from HHV-6B but that it is very different indeed: differences in mode of transmission, prevalence, types of infection, types of cells infected etc. HHV-6A, for instance, appears to be more commonly found in the cerebrospinal fluid (CSF) of AIDS and multiple sclerosis patients while HHV-6B is more frequently found in the cerebrospinal fluid (CSF) of healthy controls (Ahlqvist et al.
An in vitro study found HHV-6A but not HHV-6B was able to infect, kill and establish a latent infection in nerve cells called oligodendrocytes (Ahlqvist et al. A recent study employing real-time PCR found HHV-6B was found in most healthy controls, transplant and AIDS patients.
HHV-6B is believed to hide out in its latent phase in PBMCs, monocytes and the bone marrow progenitor cells. The HHV6 genome has been detected in brain, liver, skin, lungs, kidneys, heart, tonsils, salivary glands, esophagus, etc. HHV-6A is able to produce productive infections in T-helper cells, the same cells HIV targets, and it upregulates the expression of the primary HIV receptor CD 4. Since one of the genes plays a crucial role in switching EBV from latency to activity, HHV-6 has been proposed to reactivate EBV (Flammand et al.
Found in many parts of the brain, HHV-6 has been proposed to be a co-factor in at least nine neurological diseases including Gullain-Barre Syndrome, Bell’s palsy and multiple sclerosis.
As noted earlier, most cases of HHV-6 reactivation are benign; even though the virus is present and replicating, patients remains asymptomatic in most cases. The incidence of HHV-6B infection in both febrile seizure patients and healthy controls is, however, the same and some febrile seizure patients show no evidence of HHV-6 CNS infection (Dewhurst 2004). These patients generally demonstrated an abnormal cerebrospinal fluid profile (increased protein levels and white blood cell counts) (Tavokoli et al.
While both HHV-6A and B can infect astrocytes only HHV-6A is able to establish a productive infection in them.
High glutamate levels due to poorly performing HHV-6A infected astrocytes have been proposed to explain the lesions seen in MS. A recent in vitro study indicating HHV-6 is able to infect, replicate in and profoundly alter the morphology of GPCs suggested it may play a role in the demylinating process in MS (Dietrich et al.
HHV-6 enters cells through a ubiquitous protein called CD 46 that spans the outer membranes on almost all cells.
A parallel down regulation by HHV-6 of another receptor (CD3) involved in T-cell stimulation could result in immune suppression.


Our professionally produced segments feature people-focused stories covering medical advances and compelling general health information. Developing an awareness of prodromal symptoms is one way to try to reduce the chances of transmitting virus to another person.
Pathologic Findings The resected left lung weighed 230 g and the upper lobe appeared Bilgen EJ, Weimar W. Keywords Nasopharyngeal carcinoma, Epstein–Barr virus, Chemoradiotherapy, Induction They are often diagnosed late because as the symptoms are subtle in the early stage of disease. A capsid is constructed from identical subunits called capsomers, which are made of protein.
To start contributing, enable JavaScript by changing your browser options, then try again. Clinical Assistant Professor Division Of …Taken off Valcyte 6 weeks ago per protocol. HHV-6A was more commonly found in patients with central nervous system (CNS) dysfunctions (Boutolleau et.al.
It is believed to make its way to the brain on board T lymphocytes able to penetrate the blood:brain barrier. This limits the amount of virus present in the bloodstream and has complicated efforts to characterize its effects.
HHV-6B reactivation commonly occurs (25-75%) during these procedures and much HHV-6 research is concentrated on organ transplantation (De Bolle et al. Bone marrow suppression, transplant rejection, liver failure, pneumonitis and encephalitis may, however, be associated with HHV-6 reactivation in a small percentage of transplant patients. A PCR finding of HHV-6B DNA in the cerebrospinal fluid (CSF) does not, therefore, necessarily indicate a significant pathological process is occurring. Several recent studies have concluded, though, that HHV-6B is the likely cause of CNS damage (encephalopathy, etc.) in some children (Mannonen et al. Astrocytes provide a protective function through their uptake of the amino acid glutamate, an excitatory neurotransmitter able to cause cell death (‘excitotoxicity’) at high levels. This transmembrane protein protects them from being attacked during complement activation and plays a role in T-cell stimulation and nitric oxide (NO) production by macrophages. HHV-6 infected dendritic cells demonstrated a marked reduction in their ability to stimulate T cells and were associated with a ‘trend’ towards reduced TNF-a and increased IL-10 production (Smith et al.
Researchers proposed that the low blood flow to the basal ganglia in a case of HHV-6 encephalopathy was due to an HHV-6 caused vasculitis. A recent study indicated HHV-6A is able to induce cellular fusion simply by binding with the CD 46 protein. Human herpesvirus type 6 and human herpesvirus type 7 infections of the central nervous system. Stress-associated changes in the steady-state expression of latent Epstein-Barr virus: implications for chronic fatigue syndrome and cancer.
A six-month trial of valacyclovir in the Epstein-Barr virus subset of chronic fatigue syndrome: improvement in left ventricular function. The natural history and laboratory diagnosis of human herpesvirus-6 and -7 infections in the immunocompetent. Research on therapeutic human herpes virus 6 (HHV-6) and for Epstein–Barr virus (EBV). Most studies, however, still collapse the distinction between the two and simply study ‘HHV-6’ (Mirandola et.
An ex vivo study found HHV-6A to be more effective in mounting productive infections in cytotoxic T-cells and was more able to easily infect natural killer cells (NK) (Grivel et al. 2005). Primary Infection – HHV-6B is spread in the saliva and almost everyone carries the virus by their second year. Controversy and dissatisfaction with the current testing methodologies suggests that the true extent of HHV-6 infection is unknown.
CNS complications were significantly more likely in liver transplant patients with evidence of HHV-6 reactivation than in those without it. HHV-6B DNA has been found in the CSF of immunocompromised patients who did not display neurological symptoms (Dewhurst 2004).
Reduced glutamate uptake in HHV-6A infected astrocytes suggests HHV-6A could cause central nervous system cell death. The authors noted, however, that several neurotropic viruses are able to disrupt cell functioning without altering cell survival.
Since epithelial and endothelial cells appear most at risk from this process it is possible HHV-6 can alter blood vessel functioning as it travels through the blood stream.
Differential tropism of human herpesvirus 6 (HHV-6) variants and induction of latency by HHV-6A in oligodendrocytes. Intrathecal antibody (IgG) production against human herpesvirus type 6 occurs in about 20% of MS patients and might be linked to a polyspecific B-cell response.
Primary human herpesvirus-6 infection in the central nervous system can cause severe disease. Host RangeA cell has to have a specific structure or receptor on its surface for a virus to be able to attach to it. Treatment is experimental at this time, but anti-viral drugs or beta interferon may be tried. A recent study utilizing real-time PCR found 17% of samples from bone marrow transplant patients tested positive for HHV-6 (97% – HHV-6B) (Reddy and Manna 2005). As in AIDS, HCMV patients often exhibit HHV-6 reactivation but it does not appear to negatively affect the progression of their disease (Caserta et al. Tavokoli suggests, however, that in patients with the appropriate clinical presentation positive PCR tests of the spinal fluid are highly significant (Tavokoli et al. Hyde that vasculitis of the CNS and other parts of the body plays a major role in CFS (Click here). Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients. Identification of human herpesvirus 6 variants A and B by primer-specific real-time PCR may help to revisit their respective role in pathology. A chronic illness characterized by fatigue, neurologic and immunologic disorders and active herpesvirus type 6 infection.


Human herpesvirus 6 (HHV-6) induces dysregulation in glutamate uptake and transporter expression in astrocytes. Apoptotic effects of human herpesvirus -6A on glia and neurons as potential triggers for central nervous system autoimmunity. Human herpesvirus 6 variant A but not variant B induces fusion from without in a variety of human cells through a human herpesvirus 6 entry receptor, CD 46.
Multiple co-infections (Mycoplasma, Chlamydia, human herpes virus-6) in blood of chronic fatigue syndrome patients: association with signs and symptoms.
Early and late HHV-6 transcripts in multiple sclerosis lesions and normal appearing white matter. Quantitative detection and differentiation of human herpesvirus 6 subtypes in bone marrow transplant patients by using a single real-time polymerase chain reaction assay. Viral replication-independent blockade of dendritic cell maturation and interleukin-12 production by human herpesvirus 6.
Human herpesvirus 6 and Chlamydia pneumoniae as etiologic agents in multiple sclerosis – a critical review. Detection and typing of HHV-6 by molecular methods in specimens from patients diagnosed with encephalitis or meningitis.
Ablashi asserts that HHV-6A is the predominant strain in CFS, multiple sclerosis (MS) and AIDS patients.
Primary HHV-6B infection in children is, however, believed to cause febrile seizure and have severe CNS complications (encephalitis, meningitis, ataxia, learning disabilities) in rare cases.
A 2006 study finding that HHV-6A is able to induce oligodendrocytes to commit suicide provided another mechanism of HHV-6A induced cell death (Gardell et al. In vitro studies that indicate HHV-6 can infect the endothelial cells which line the blood vessels suggest it could induce vasculitis. Genomic polymorphism, growth properties and immunologic variations in human herpes virus-6 isolates.
Infection with an endemic human herpesvirus disrupts critical glial precursor cell properties. Nor does HHV-6 infection appear to increase the risk of mycoplasma or chlamydiae infection in chronic fatigue syndrome patients (Nicholson et al.
Animal virus replication is MORE complex than phage replication because host cells are more complex2. Most DNA viruses bud off of the nucleus and most RNA viruses multiply and are released from the cytoplasm.
Larry Brilliant telling the fascinating tale of the eradication of smallpox:Cowpox Cowpox virus, from the genus Orthpoxvirus, is another poxvirus that causes human disease through zoonosis. EpidemiologyCowpox virus has been found only in Europe and in adjacent parts of the former Soviet Union.
Despite its name, the reservoir hosts of cowpox virus are rodents, from which it can occasionally spread to cats, cows, humans, and zoo animals, including large cats and elephants. Transmission to humans has traditionally occurred via contact with the infected teats of milking cows. However, currently, infection is seen more commonly among domestic cats, from which it can be transmitted to humans.
Symptomatology and OutcomeInfection with cowpox virus in humans produces localized, pustular lesions at the site of their introduction into the skin.
The lesion is similar to that caused by vaccination, although the inflammatory response is greater. The lesions in humans usually appear on the hands: on the thumbs, the first interdigital cleft, and the forefinger. Pathology and PathogenesisThe pathology of the skin lesions caused by cowpox virus is similar to that of smallpox. The most significant pathological feature of cowpox is the presence of two types of cytoplasmic inclusion bodies: irregular B-type inclusion bodies, and numerous large, homogenous, acidophilic, A-type inclusion bodies. Management and PreventionHuman cowpox usually responds to treatment with antivaccina immunoglobulin. Usually, the lesions regress spontaneously.Identification and isolation of animals infected with cowpox can help decrease the incidence of human infections.
Attention to the newly emerging prevalence of cowpox virus among domestic cats and subsequent, directive action can also help reduce the number of human infections.
Monkeypox Human infections with monkeypox virus, from the genus Orthopoxvirus, were first observed in West and Central Africa during the early 1970s, after smallpox had already been eradicated in this region.
Although the signs and symptoms of monkeypox are very similar to those of smallpox, this virus is significantly different. This virus is a rare zoonosis found only in the small villages of the tropical rain forests of western and central Africa, with cases mostly reported in Zaire. As a result of intensive surveillance efforts conducted by the World Health Organization, only 400 cases were reported worldwide from the time infection by monkeypox virus was first observed in 1970 to the time when surveillance ceased in 1986.Monkeypox virus is believed to be transmitted through direct contact with wild animals killed for food, such as squirrels and monkeys.
Incubation period Incubation period is between 10-14 days, usually 12 days.Pathogenesis and PathologyVery similar to smallpox where the virus replicates in lymphoid tissues, however, the viral entry occurs by small lesions and it may also occur via respiratory tract.
Prevention and ManagementVaccination with smallpox vaccine immunizes against monkeypox, but it is not justified since the disease is so rare. In the United States, Vaccinia vaccination is recommended for laboratory workers who directly handle cultures or animals infected with monkeypox virus. Management for monkeypox involves effective surveillance efforts such as those undertaken by the World Health Organization prior to 1980. An important thing to remember is that unlike smallpox, human monkeypox has a lower capacity for human spread.
The bumps may be pink, pearly-white, or the same color as the rest of the skin in the affected area. Often the infection goes unnoticed, but child may have a low-grade fever and a bright red rash on the cheeks. This virus can be more dangerous in children with immunodeficiency or sickle-cell anemia, because it destroys red blood stem cells.The adeno-associated virus (A-AV) is another example of a defective virus that cannot replicate in the host cell without function of a helper cell.



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