HHV-6 and HHV-7 primary infections cause roseola infantum, which is a common pediatric infection. Most infections are due to HHV-6, and HHV-7 is considerably less common. This condition, also referred to as the 6th disease or as exantheum subitum, manifests in infants aged six to twelve months, with 90% of cases occurring in children under the age of two.
Patients infected with the B type of HHV-6 typically manifests through the onset of a high-grade fever which goes up to 104 Degrees Fahrenheit in temperature for 3-5 days. Children affected, will have a quick defervescence of fever along with the onset of a nonpruritic, pink papular rash over the trunk. This illness is prevalent worldwide and has been identified as the cause of 10%-45% of febrile illnesses in babies.
During the febrile phase of the illness, 15% of children will also experience an acute febrile seizure because of the high fever and virus’ ability to cross the blood-brain barrier. This illness is generally treated symptomatically. In immunocompetent people, HHV-6 will usually remain dormant, but in immunocompromised patients, it can be a significant cause of mortality and morbidity.
Epidemiology
HHV-6 has been identified as the causative agent of febrile sickness in 10%-45% of infants in the US. A population-based study from 2005 found that 40% of HHV-6 infections manifest by the age of 12 months, and 77% by the age of 24 months.
According to this study, the virus is found in both genders, however it is more prevalent in children or females who have older siblings. The virus is more prevalent during fall and spring.
Transmission of this illness happens predominantly through respiratory droplets containing saliva.
Anatomy
Pathophysiology
During the first infection, HHV-6 replicates more frequently in leukocytes and salivary glands; hence, it is present in saliva. High levels of tissue inhibitor of metalloproteinases 1 and metalloproteinase 9 in the serum of babies infected with HHV-6 have been linked to disruption of the blood-brain barrier, which may contribute to the development of febrile seizures.
Early CNS invasion has also been demonstrated in this illness. Two variants of human herpesvirus 6 exist: A and B. HHV-6B is the most common cause of roseola infantum. Currently, HHV-6A is not linked to any disease.
It has been demonstrated that Human Herpes Virus-6 replicates most efficiently in CD4+ T cells and the average incubation period is between 9-10 days. Following an acute infection, HHV-6 is latent in monocytes and lymphocytes, with brain tissue and salivary glands retaining the chronic HHV-6 infection.
Etiology
HHV-6 is the primary cause of roseola infantum. It is a betaherpesvirus which is related to HCMV and HHV-7 (another cause of this illness). These betaherpesviruses display less tropism than other viruses from the Herpesviridae family.
HHV-6 has a double-stranded DNA genome that is flanked by direct terminal repeats with hexanucleotide repetitions. It is believed that these repetitions contribute to the preservation of the viral genome in latently infected cells.
Genetics
Prognostic Factors
This illness has a great prognosis. As roseola infantum is a self-limited condition it only causes a few long-term side-effects.
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK448190/
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HHV-6 and HHV-7 primary infections cause roseola infantum, which is a common pediatric infection. Most infections are due to HHV-6, and HHV-7 is considerably less common. This condition, also referred to as the 6th disease or as exantheum subitum, manifests in infants aged six to twelve months, with 90% of cases occurring in children under the age of two.
Patients infected with the B type of HHV-6 typically manifests through the onset of a high-grade fever which goes up to 104 Degrees Fahrenheit in temperature for 3-5 days. Children affected, will have a quick defervescence of fever along with the onset of a nonpruritic, pink papular rash over the trunk. This illness is prevalent worldwide and has been identified as the cause of 10%-45% of febrile illnesses in babies.
During the febrile phase of the illness, 15% of children will also experience an acute febrile seizure because of the high fever and virus’ ability to cross the blood-brain barrier. This illness is generally treated symptomatically. In immunocompetent people, HHV-6 will usually remain dormant, but in immunocompromised patients, it can be a significant cause of mortality and morbidity.
HHV-6 has been identified as the causative agent of febrile sickness in 10%-45% of infants in the US. A population-based study from 2005 found that 40% of HHV-6 infections manifest by the age of 12 months, and 77% by the age of 24 months.
According to this study, the virus is found in both genders, however it is more prevalent in children or females who have older siblings. The virus is more prevalent during fall and spring.
Transmission of this illness happens predominantly through respiratory droplets containing saliva.
During the first infection, HHV-6 replicates more frequently in leukocytes and salivary glands; hence, it is present in saliva. High levels of tissue inhibitor of metalloproteinases 1 and metalloproteinase 9 in the serum of babies infected with HHV-6 have been linked to disruption of the blood-brain barrier, which may contribute to the development of febrile seizures.
Early CNS invasion has also been demonstrated in this illness. Two variants of human herpesvirus 6 exist: A and B. HHV-6B is the most common cause of roseola infantum. Currently, HHV-6A is not linked to any disease.
It has been demonstrated that Human Herpes Virus-6 replicates most efficiently in CD4+ T cells and the average incubation period is between 9-10 days. Following an acute infection, HHV-6 is latent in monocytes and lymphocytes, with brain tissue and salivary glands retaining the chronic HHV-6 infection.
HHV-6 is the primary cause of roseola infantum. It is a betaherpesvirus which is related to HCMV and HHV-7 (another cause of this illness). These betaherpesviruses display less tropism than other viruses from the Herpesviridae family.
HHV-6 has a double-stranded DNA genome that is flanked by direct terminal repeats with hexanucleotide repetitions. It is believed that these repetitions contribute to the preservation of the viral genome in latently infected cells.
This illness has a great prognosis. As roseola infantum is a self-limited condition it only causes a few long-term side-effects.
https://www.ncbi.nlm.nih.gov/books/NBK448190/
medtigo
Roseola Infantum
Updated :
July 15, 2022
HHV-6 and HHV-7 primary infections cause roseola infantum, which is a common pediatric infection. Most infections are due to HHV-6, and HHV-7 is considerably less common. This condition, also referred to as the 6th disease or as exantheum subitum, manifests in infants aged six to twelve months, with 90% of cases occurring in children under the age of two.
Patients infected with the B type of HHV-6 typically manifests through the onset of a high-grade fever which goes up to 104 Degrees Fahrenheit in temperature for 3-5 days. Children affected, will have a quick defervescence of fever along with the onset of a nonpruritic, pink papular rash over the trunk. This illness is prevalent worldwide and has been identified as the cause of 10%-45% of febrile illnesses in babies.
During the febrile phase of the illness, 15% of children will also experience an acute febrile seizure because of the high fever and virus’ ability to cross the blood-brain barrier. This illness is generally treated symptomatically. In immunocompetent people, HHV-6 will usually remain dormant, but in immunocompromised patients, it can be a significant cause of mortality and morbidity.
HHV-6 has been identified as the causative agent of febrile sickness in 10%-45% of infants in the US. A population-based study from 2005 found that 40% of HHV-6 infections manifest by the age of 12 months, and 77% by the age of 24 months.
According to this study, the virus is found in both genders, however it is more prevalent in children or females who have older siblings. The virus is more prevalent during fall and spring.
Transmission of this illness happens predominantly through respiratory droplets containing saliva.
During the first infection, HHV-6 replicates more frequently in leukocytes and salivary glands; hence, it is present in saliva. High levels of tissue inhibitor of metalloproteinases 1 and metalloproteinase 9 in the serum of babies infected with HHV-6 have been linked to disruption of the blood-brain barrier, which may contribute to the development of febrile seizures.
Early CNS invasion has also been demonstrated in this illness. Two variants of human herpesvirus 6 exist: A and B. HHV-6B is the most common cause of roseola infantum. Currently, HHV-6A is not linked to any disease.
It has been demonstrated that Human Herpes Virus-6 replicates most efficiently in CD4+ T cells and the average incubation period is between 9-10 days. Following an acute infection, HHV-6 is latent in monocytes and lymphocytes, with brain tissue and salivary glands retaining the chronic HHV-6 infection.
HHV-6 is the primary cause of roseola infantum. It is a betaherpesvirus which is related to HCMV and HHV-7 (another cause of this illness). These betaherpesviruses display less tropism than other viruses from the Herpesviridae family.
HHV-6 has a double-stranded DNA genome that is flanked by direct terminal repeats with hexanucleotide repetitions. It is believed that these repetitions contribute to the preservation of the viral genome in latently infected cells.
This illness has a great prognosis. As roseola infantum is a self-limited condition it only causes a few long-term side-effects.
https://www.ncbi.nlm.nih.gov/books/NBK448190/
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