High Prevalence of Torque Teno (TT) Virus in Classical Kaposi's Sarcoma
Service de Dermatologie, Hopital Saint Eloi, CHU Montpellier, Laboratoire de Virologie, France.Acta Dermato Venereologica (Impact Factor: 3.03). 02/2007; 87(1):14-7. DOI: 10.2340/00015555-0188
Human herpes virus 8 infection is the primary and necessary factor in the development of Kaposi's sarcoma, but is not sufficient per se to trigger the onset of the disease. In order to search for virological cofactors associated with the occurrence of the disease, we investigated the prevalence of active infection by two newly discovered viruses, hepatitis G virus and TT virus, among patients with classical Kaposi's sarcoma. Serum of 24 patients with Mediterranean Kaposi's sarcoma was investigated using polymerase chain reaction and compared with that of 68 healthy subjects. Cutaneous samples from patients with Kaposi's sarcoma and healthy subjects were investigated for TT virus DNA. No patient had serum markers for hepatitis G virus. TT virus DNA was present in the serum of 21/24 (87.5%) patients and 32/68 (47%) controls (p=0.002). TT virus DNA was present in the lesional skin of 5/18 patients with Kaposi's sarcoma (27.7%), but not in the skin of controls. TT virus might play a role as a cofactor in the clinical emergence of Kaposi's sarcoma in patients infected with Human herpes virus 8, perhaps by immunosuppressive effects or by a common transmission pathway for these two viruses.
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ABSTRACT: Kaposi sarcoma (KS) remains a challenge. Its classic or Mediterranean form tends to be benign. In transplant recipients it may be less so. As part of the AIDS pandemic, of which it was an original defining component, it may be life-threatening. It is due to human herpesvirus-8, which is necessary but not sufficient to produce the disease. KS has a low prevalence in the general population of the United States and United Kingdom, with an intermediate rate in Italy and Greece, and a high one in parts of Africa. In Italy, hot spots include its southern regions, the Po River Valley, and Sardinia, possibly related to a high density of blood-sucking insects. An important challenge is to treat KS patients without immunocompromising them. The potential of effective anti-herpes virus therapy and the use of sirolimus in transplantation recipients have added new opportunities for KS prevention. LEARNING OBJECTIVES: At the conclusion of this learning activity, participants should be able to provide the most recent information about Kaposi sarcoma in the context in which it occurs. Its classic or Mediterranean form, its pattern in transplant recipients and others iatrogenically immunosuppressed, and its occurrence as a potentially life-threatening part of the AIDS pandemic will be stressed. Its etiology and transmission will be discussed in detail to facilitate understanding of Kaposi sarcoma and of human herpesvirus-8 infection in the general population of the United States and United Kingdom, in Italy and Greece, and in certain parts of Africa. Its therapy, including the concept of doing it without immunocompromising the patient, will be stressed. New opportunities for Kaposi sarcoma prevention will also be discussed.
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ABSTRACT: Current clinical studies on human annelloviruses infections are directed towards finding an associated disease. In this review we have emphasized the many similarities between human anellovirus and avian circoviruses and the cell and tissue types infected by these pathogens. We have done this in order to explore whether knowledge acquired from natural and experimental avian infections could reflect and be extrapolated to the less well-characterized human annellovirus infections. The knowledge gained from the avian system may provide suggestions for decoding the enigmatic human anellovirus infections, and finding the specific disease or diseases caused by these human anellovirus infections. Each additional parallelism between chicken anemia virus (CAV) and Torque teno virus (TTV) further strengthens this premise. As we have seen information from human infections can also be used to better understand avian infections as well. Increased attention must be focused on the "hidden" or unrecognized, seemingly asymptomatic effects of circovirus and anellovirus infections. Understanding the facilitating effect of these infections on disease progression caused by other pathogens may help to explain differences in outcome of complicated poultry and human diseases. The final course of a pathogenic infection is determined by variations in the state of health of the host before, during and after contact with a pathogen, in addition to the phenotype of the pathogen and host. The health burden of circoviridae and anellovirus infections may be underestimated, due to lack of awareness of the need to search past the predominant clinical effect of identified pathogens and look for modulation of cellular-based immunity caused by co-infecting circoviruses, and by analogy, human anneloviruses.
Chapter: Chicken Anemia Virus[Show abstract] [Hide abstract]
ABSTRACT: Chicken anemia virus (CAV), the only member of the genus Gyrovirus of the Circoviridae, is a ubiquitous pathogen of chickens and has a worldwide distribution . CAV shares some similarities with Torque teno virus (TTV) and Torque teno mini virus (TTMV) such as coding for a protein inducing apoptosis and a protein with a dual-specificity phosphatase. In contrast to TTV, the genome of CAV is highly conserved. Another important difference is that CAV can be isolated in cell culture. CAV produces a single polycis-tronic messenger RNA (mRNA), which is translated into three proteins. The promoter-enhancer region has four direct repeats resembling estrogen response elements. Transcription is enhanced by estrogen and repressed by at least two other transcription factors, one of which is COUP-TF1. A remarkable feature of CAV is that the virus can remain latent in gonadal tissues in the presence or absence of virus-neutralizing antibodies. In contrast to TTV, CAV can cause clinical disease and subclinical immunosuppression especially affecting CD8 + T lymphocytes. Clinical disease is associated with infection in newly hatched chicks lacking maternal antibodies or older chickens with a compromised humoral immune response.
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