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Human Herpesvirus 6 Infection

Human Herpesvirus 6 Infection

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Human herpesvirus 6 (HHV-6) was the sixth herpesvirus discovered. Isolated in 1986 during attempts to find novel viruses in patients with lymphoproliferative diseases, HHV-6 is now recognized as a T-cell lymphotropic virus with high affinity for CD4 lymphocytes. [1, 2]

A beta herpesvirus (like cytomegalovirus [CMV] and human herpesvirus 7 [HHV-7]), HHV-6 comprises 2 forms, A and B; as of 2012, HHV-6A and HHV-6B are officially considered distinct species rather than variants of 1 species. HHV-6B causes the childhood illness roseola infantum, whereas HHV-6A has been isolated mainly in immunocompromised hosts. Specific manifestations of HHV-6A infection are still undefined. However, both HHV-6A and HHV-6B may be pathogenic in the settings of transplantation and AIDS. (See Pathophysiology and Etiology.)

Primary HHV-6B infection usually occurs in infants and is the most common cause of fever-induced seizures in children aged 6-24 months. Acute HHV-6 infection is rare in immunocompetent adults but may manifest as a mononucleosislike illness characterized by fever, lymphadenopathy, and hepatitis or encephalitis, with negative test results for CMV or Epstein-Barr virus (EBV). [3]

After primary infection, HHV-6 remains latent unless the immune system is compromised, at which time the virus may reactivate. HHV-6 remains latent in lymphocytes and monocytes and persists at low levels in cells and tissues. In immunocompetent hosts, this persistent infection is generally of no consequence. Isolated cases of pulmonary failure in immunocompetent patients have been attributed to HHV-6 when no other pathogens have been isolated; however, such cases are not common, and no causal relation has been established. [4]

In immunosuppressed hosts, HHV-6A reactivation is associated with a worse outcome. [5, 6] Such reactivation occurs in 33-48% of patients undergoing hematopoietic stem-cell transplantation. For example, in these patients, reactivation of HHV-6 has been associated with CMV reactivation and increased severity of CMV disease.

Other clinical conditions associated with HHV-6 reactivation in this population include hepatitis, idiopathic pneumonitis, bone-marrow suppression, encephalitis, fever and rash, graft versus host disease (GVHD), and delayed engraftment. Although reactivation of HHV-6 accounts for most infections, transmissions of HHV-6 with the donor allograft, solid organ, or hematopoietic stem cell have also been reported. [7, 8, 9]

In patients infected with HIV, HHV-6 infection may up-regulate HIV replication and hasten the progression toward AIDS. HHV-6 also has been implicated in the pathogenesis of white-matter demyelination in persons with AIDS dementia complex; however, causality has not been proven.

HHV-6 has been isolated from various tissues, cells, and fluid in association with the following conditions:

Kikuchi lymphadenitis

Lymphoma

Lymphadenopathy

Drug-induced hypersensitivity syndrome (DIHS), [10] or drug reaction with eosinophilia and systemic symptoms (DRESS)

Sjögren syndrome

Sarcoidosis

Systemic lupus erythematosus

Chronic fatigue syndrome (CFS)

Guillain-Barré syndrome

Multiple sclerosis (MS)

A causal relation has not been yet been established between HHV-6 and these conditions.

The great majority of HHV-6 infections are silent or appear as a general mild febrile illness (see Presentation). Laboratory diagnosis is rarely required in patients who are immunocompetent; most often, HHV-6 infection is diagnosed on the basis of its clinical features (see DDx and Workup).

No specific treatment for HHV-6 infection has been established. Treatment varies according to the presenting clinical situation and is usually unnecessary with primary infection in immunocompetent hosts. Supportive measures are the basis of care. Some infants may require hospitalization for atypical presentations. Antivirals such as ganciclovir and foscarnet have been suggested as possible therapies for acute disease, but they remain unproven. No vaccine exists. (See Treatment.)

For patient education resources, see the Bacterial and Viral Infections Center and the Children’s Health Center, as well as Mononucleosis and Skin Rashes in Children.

HHV-6 belongs to the Betaherpesvirinae subfamily and to the Roseolovirus genus. The virion particle has the typical structure of a herpesvirus, with a central core containing the viral DNA, a capsid, and a tegument layer that, in turn, is surrounded by a membrane.

At the molecular level, HHV-6 encodes proteins similar to immune mediators in the chemokine family. The functional chemokine is encoded by an open reading frame U83; U12 and U51 encode the 7 transmembrane proteins analogous to the chemokine receptors. This molecular mimicry seems to help HHV-6 in immune invasion and to contribute to long latency in the host cells. [11]

The exact mode by which HHV-6 is transmitted has yet to be elucidated fully. Studies indicate that primary HHV-6B infection is acquired during the first 24months of life. Children likely acquire infection through contact with adult caretaker saliva or from older siblings. DNA restriction enzyme profile studies have shown mothers’ isolates to be genetically similar to their infants’. Vertical transmission of HHV 6 has been documented; however, this mode of transmission represents only 1-2% of all births. [12]

HHV-6 chromosomal integration in immunocompetent patients has been found to result in high levels of viral DNA in blood, sera, and hair follicles. [13] These characteristically high HHV-6 DNA levels in chromosomal integration should be considered in the effort to establish accurate laboratory diagnosis methods.

In vivo, HHV-6 primarily infects and replicates in CD4 lymphocytes. The cellular receptor is CD46, a 52- to 57-kd type 1 transmembrane glycoprotein expressed on the surface of all cells. The cell attachment protein of HHV-6 has not been identified. Entry occurs through receptor-mediated endocytosis. Subsequent stages of viral replication are similar to those of CMV.

During acute infection, replication occurs in lymphocytes, macrophages, histiocytes, endothelial cells, and epithelial cells. In vitro studies have demonstrated that HHV-6 also can replicate in glial cells. The virus is believed to invade the central nervous system (CNS), which may lead to such CNS complications as seizures and encephalitis.

HHV-6 causes direct cytolysis; this effect may be responsible for roseola, as well as the heterophile-negative mononucleosislike picture of acute infection.

HHV-6 has been shown to upregulate CD4 lymphocytes and natural killer (NK) cells and to downregulate CD3 T cells. HHV-6 infection has been reported to induce down-regulation of CXC chemokine receptor 4 in CD4+ T lymphocytes. [14] NK cells seem to play a major role in resolving acute-phase HHV-6 infection [15] ; specific lymphocyte activity develops later. The lymphoproliferative response to phytohemagglutinin ratios suggests that HHV-6 infection has some impact on host T-cell immunity during the course of exanthema subitum.

HHV-6 is also a powerful inducer of cytokines and triggers the release of interferon alfa, tumor necrosis factor, and interleukin-1b, thus potentially playing a role in the pathogenesis of HIV disease and other immunocompromised states. HHV-6 may also alter the natural history of other viral infections, such as those with CMV, EBV, and human papillomavirus (HPV).

HHV-6 antigen has been found in the nuclei of oligodendrocytes in the plaques of patients with MS. [16] Researchers have also found a strong association between anti–HHV-6 immunoglobulin M (IgM) antibodies and early MS in comparison with healthy control subjects and progressive MS.

Some theorize that viral infection plays a role in the pathogenesis of MS through potential molecular mimicry. Cross-reactivity between myelin basic protein and HHV-6 has been suggested. [17] Thus, the host response may be responsible, rather than the viral infection itself. However, further investigation is needed before the role of HHV-6 in MS can be fully defined. [18]

HHV-6 is the virus that most commonly causes the childhood disease roseola. [19] It includes 2 genetically distinct forms: HHV-6A and HHV-6B. These 2 forms were originally considered variants of a single species but are now considered separate species. [20] HHV-6B has been associated with a variety of viral illnesses, including exanthema subitum (roseola infantum), mononucleosis syndromes, focal encephalitis, and pneumonitis. [21] This virus shows the closest homology with CMV and HHV-7.

HHV-6B infection in infants is the most common cause of fever-induced seizures. In a prospective study involving children aged 1 month to 5 years, HHV-6B was found to be commonly associated with febrile status epilepticus (as was HHV-7, albeit to a lesser degree). [22]

Infection in adults is seen primarily in immunocompromised hosts who have undergone solid-organ or stem cell transplantation or in those with HIV infection. [23, 24]

To elucidate the roles of HHV-6 and HHV-7 in pityriasis rosea (PR), their DNA load in plasma, peripheral blood mononuclear cells (PBMCs), and tissues was evaluated by using a calibrated quantitative real-time polymerase chain reaction (PCR) assay. [25] In addition, HHV-6– and HHV-7–specific antigens in skin were evaluated by means of immunohistochemistry (IHC), and anti–HHV-7 neutralizing activity was assessed with a syncytia-inhibition test.

HHV-6 and HHV-7 DNA were found in 17% and 39% of PR plasmas, respectively, but in no controls. [25] HHV-6 levels in PBMCs were not higher in PR patients than in controls. HHV-6 and HHV-7 antigens were detected only in PR skin (17% and 67% of instances, respectively), presumably indicating a productive infection. These and other data strongly suggest a causal association between PR and active HHV-7 or, to a lesser extent, HHV-6 infection.

The reactivation of herpesviruses, including HHV-6 and EBV, is linked with a potentially serious drug eruption known as DRESS (drug reaction with eosinophilia and systemic symptoms; also referred to as DIHS). [26] A report of high-level HHV-6 viremia associated with the onset of Stevens-Johnson syndrome suggests an association. [27]

As noted (see Pathophysiology), the role of HHV-6 in MS remains controversial. [18]

An association between HHV-6 reactivation and CFS has been proposed. A high proportion of patients with CFS are infected with HHV-6 but have a low viral load. Study results to date have not supported HHV-6 reactivation in patients with CFS, though further investigation is required. [28]

Good prospective studies in patients with encephalitis, posttransplant pneumonia, and MS are needed.

It has been speculated that HHV-6 infection may act as an inducer of sporadic porphyria cutanea tarda, triggering it to become apparent clinically. [29]

HHV-6 infection is ubiquitous. HHV-6B is the cause of most symptomatic HHV-6 infections. Although evidence of past HHV-6 infection is found in most people, initial infection usually occurs within the first 2 years of life; greater than 90% seropositivity reported in children older than 2 years. Roseola is estimated to affect as many as 30% of all children and is most common in spring and fall.

HHV-6 has a worldwide distribution. In an HIV-1 endemic region of sub-Saharan Africa, the predominant form in infant infections was found to be HHV-6A. [30] In Europe and Japan, as in the United States, HHV-6B is the agent mainly responsible for infant infection; HHV-6A appears to be rare.

Seroprevalence is almost 100% in Europe and is close to 100% in the rest of the world—with certain exceptions, such as Morocco, which has 20% seroprevalence. Virus shedding evaluated by PCR in the saliva of healthy adults in Rio de Janeiro, Brazil, detected an HHV-6 prevalence of 9.8%, with HHV-6A detected in 7.1% of the samples and HHV-6B in 2.7%. [31]

HHV-6 infection most commonly occurs after maternal antibodies have waned, usually between the ages of 6 months and 3 years (average, 9 months). The virus is shed in and probably spread through saliva of asymptomatic seropositive children.

Serologic studies demonstrate that HHV-6 infects approximately 90% of children by the age of 2 years. [32] A prospective study found that HHV-6 was acquired in infancy, was usually symptomatic, and often resulted in a medical evaluation. However, only a minority of these patients developed roseola or febrile seizures with primary HHV-6 infection. Older siblings and other care takers appeared to be a source of HHV-6 transmission. [12, 32]

Primary HHV-6 infection is rare in adults. However, reactivation can occur at any age.

HHV-6 infection has no sexual predilection and may occur in people of all races.

HHV-6 infections are mainly uncomplicated and have a self-limited course. They are usually asymptomatic. Even when HHV-6 leads to roseola, it is a mild illness in children who are immunocompetent. It usually resolves without any treatment; however, in some rare cases, patients who are immunocompetent may develop additional symptoms, including respiratory distress, seizures, and multiorgan involvement. One infection usually provides lifetime immunity, though HHV-6 may reactivate in patients who are immunocompromised.

Rarely, HHV-6 can be associated with fatal dissemination and death; 8 fatal cases have been reported. The causes of death were encephalitis, hepatitis, [33] sudden death in infancy, hemophagocytic lymphocytosis, and disseminated infections. In studies by Prezioso et al and Hoang et al, atypical monocyte infiltrate was found in multiple organs, including the brain, spleen, lungs, liver, heart, renal cortex, lymph nodes, and intestine. [34, 35]

In adults who are immunosuppressed (eg, those with AIDS), HHV-6A is a major source of morbidity and mortality, especially in those who do not take antiretroviral therapy; disseminated organ involvement and death can occur. In adults who are immunosuppressed because of undergoing a transplant, HHV-6 infection may cause multiorgan system involvement, accelerate organ rejection, and lead to death.

In adults who are immunocompetent, primary infection or reactivation with HHV-6 can produce a mononucleosislike illness and, more rarely, severe disease, including encephalitis.

HHV-6 may be associated with various complications, as follows:

HHV-6B infection is the most common cause of febrile seizures in childhood (age 6-24 months)

Encephalitis may develop in children with HHV-6 infection

HHV-6 has a possible role in CNS infections and demyelinating conditions

HHV-6 infection may increase the severity of CMV infection in immunocompromised and transplant populations

HHV-6 has a possible role in lymphoproliferative syndromes

HHV-6A infection induces bone marrow suppression, respiratory failure, GVHD, and encephalitis in patients undergoing hematopoietic stem cell or solid-organ transplantation [36, 37]

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Michelle R Salvaggio, MD, FACP Assistant Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine; Medical Director of Infectious Diseases Institute, Director, Clinical Trials Unit, Director, Ryan White Programs, Department of Medicine, University of Oklahoma Health Sciences Center; Attending Physician, Infectious Diseases Consultation Service, Infectious Diseases Institute, OU Medical Center

Michelle R Salvaggio, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Received honoraria from Merck for speaking and teaching.

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Ruchir Agrawal, MD Chief, Allergy and Immunology, Aurora Sheboygan Clinic

Ruchir Agrawal, MD, is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, and American Medical Association

Disclosure: Nothing to disclose.

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Franklin Flowers, MD Chief, Division of Dermatology, Professor, Department of Medicine and Otolaryngology, Affiliate Associate Professor of Pediatrics and Pathology, University of Florida College of Medicine

Franklin Flowers, MD, is a member of the following medical societies: American College of Mohs Micrographic Surgery and Cutaneous Oncology

Disclosure: Nothing to disclose.

Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

Cris Jagar, MD Staff Physician, Department of Psychiatry, Trinitas Regional Medical Center

Disclosure: Nothing to disclose.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Sue J Jue, MD Associate Professor, Department of Pediatrics, Section of Infectious Diseases, East Carolina University

Disclosure: Nothing to disclose.

Ewa Koziorynska, MD Assistant Professor of Neurology, Comprehensive Epilepsy Center, State University of New York Downstate Medical Center

Ewa Koziorynska, MD is a member of the following medical societies: Sigma Xi

Disclosure: Nothing to disclose.

Leonard R Krilov, MD Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics, Professor of Pediatrics, Winthrop University Hospital

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Medimmune Grant/research funds Clinical trials; Medimmune Honoraria Speaking and teaching; Medimmune Consulting fee Consulting

Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Thomas J Marrie, MD Dean of Faculty of Medicine, Dalhousie University Faculty of Medicine, Canada

Thomas J Marrie, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, Canadian Infectious Disease Society, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Peter S Miele, MD Medical Officer, Division of Antiviral Products, US Food and Drug Administration

Peter S Miele, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Margo A Smith, MD Associate Program Director, Department of Medicine, Washington Hospital Center; Assistant Professor, Department of Internal Medicine, Section of Infectious Diseases, George Washington University

Margo A Smith, MD is a member of the following medical societies: American Society for Microbiology

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children’s Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Human Herpesvirus 6 Infection

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