The life cycle of the polyomavirus begins with the interaction of VP1 with a receptor on the cell surface and virions internalization by the cell.
Then after the endosomal transport of the virions through the cytoplasm and delivery of a viral genome to the cell nucleus, T antigens are then transcribed.
The polyomavirus replicates within the nucleus where viral DNA replication and formation of progeny virions take place.
Polyomaviruses enter the cell cytoplasm by endocytosis and are transported to the nucleus via the cytoskeleton transport machinery.
Polyomavirus is not cancerous itself although it is associated with the development of Merkel Cell carcinoma cancer and is considered to be a group 2A carcinogen.
The disease that polyomavirus causes is hemorrhagic cystitis in people who have had bone marrow transplantation and progressive multifocal leukoencephalopathy in immunocompromised people such as, by HIV infection.
The human polyomavirus is pretty common and affects between 60 percent to 90 percent of the human population worldwide especially during childhood without any known signs and symptoms.
Humans get the polyomavirus through fecal oral route or respiratory route or through sexual contact.
The polyomavirus came from specimens of immunocompromised patients and is usually first aquired in childhood and can then be reactivated and cause infection in immunocompromised people.
Most human polyoma disease is caused by BK and JC viruses which are usually acquired in childhood.
The first human polyomaviruses, BK virus (BKV) and JC virus (JCV), were also coincidently isolated in 1971 by two independent groups, BKV from the urine of a renal transplant patient who suffered from ureteral stenosis (Gardner et al., 1971) and JCV from the brain tissue of a patient with Hodgkin's lymphoma.
Polyomavirus also known as polyomaviridae is a family of viruses whose natural hosts are primarily mammals and birds.
There are eight recognized genera currently and 14 species are known to infect humans, while others, such as Simian Virus 40, have been identified in humans to a lesser extent.
The human polyomaviruses BKV and JCV are known to cause, respectively, hemorrhagic cystitis in recipients of bone marrow transplantation and progressive multifocal leukoencephalopathy in immunocompromised patients, for example, by HIV infection.
MCPyV is associated with the development of Merkel cell carcinoma (MCC) and is considered a group 2A carcinogen (probably carcinogenic to humans) by the International Agency for Research on Cancer 51.
It is accepted that PyV-associated tumors develop after the interruption of the viral life cycle.
There is no definitive treatment for APV.
Birds with mild hemorrhaging might benefit from vitamin K injections and supportive veterinary care.
Often, the disease progresses so quickly that no treatment will be effective.
The hardy, non-enveloped viruses of 40- to 45-nm diameter are likely to be transmitted by direct person-to-person contact and by exposure to contaminated surfaces, foods and water.
Very little is known about the transmission of polyomaviruses. Both BKV and JCV are frequently detected in urine.
Respiratory, sexual and fecal-oral routes of transmission are all possible.
The symptoms of the BK polyomavirus include.
Changes in vision, like blurred vision.
Changes in the color of your urine (urine that is brown or red in color)
Pain when you urinate.
Difficulty urinating.
Needing to urinate more than is normal for you.
A cough, cold, or trouble breathing.
Fever, muscle pain, or weakness.
Polyomavirus virions are about 44 nm in diameter, have icosahedral symmetry and are composed of 72 capsomeres.
The viral genome is a circular, covalently closed, supercoiled, double-stranded DNA of about 5000 bp.