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Healthy individuals can be infected with the virus and show no signs or symptoms, due to the immune system's ability to keep the infection in check. Infection is of particular concern to the immunocompromised. Cancer patients receiving chemotherapy, AIDS patients, and organ transplant patients are all at a high risk of showing signs of infection.
Herpesviruses also cause cancer in animals, especially leukemias and lymphomas. [13] Human T cell lymphotropic virus was the first human retrovirus discovered by Robert Gallo and colleagues at NIH. [20] The virus causes Adult T-cell leukemia, a disease first described by Takatsuki and colleagues in Japan [21] and other neurological diseases ...
The Epstein–Barr virus (EBV), formally called Human gammaherpesvirus 4, is one of the nine known human herpesvirus types in the herpes family, and is one of the most common viruses in humans. EBV is a double-stranded DNA virus. [2] Epstein–Barr virus (EBV) is the first identified oncogenic virus, or a virus that can cause cancer. EBV ...
More than 3.7 billion people under the age of 50 suffer from the herpes simplex virus type 1 (HSV-1), usually after catching it in childhood. ... HSV-2, which causes genital herpes.
Adenoviruses can lead to tumors in rodent models but do not cause cancer in humans; however, they have been exploited as delivery vehicles in gene therapy for diseases such as cystic fibrosis and cancer. [15] Simian virus 40 (SV40), a polyomavirus, can cause tumors in rodent models but is not oncogenic in humans. [16]
Fluid builup in the lower legs, feet and hands—also known as pedal edema— occurs because the heart’s ability to pump blood is too weak, which causes the blood to settle and accumulate in tissue.
Herpes simplex, often known simply as herpes, is a viral infection caused by the herpes simplex virus. [5] Herpes infections are categorized by the area of the body that is infected. The two major types of herpes are oral herpes and genital herpes , though other forms also exist.
The herpes simplex virus type 1 (HSV-1) mutant 1716 lacks both copies of the ICP34.5 gene, and as a result is no longer able to replicate in terminally differentiated and non-dividing cells but will infect and cause lysis very efficiently in cancer cells, and this has proved to be an effective tumour-targeting strategy.