The wart!

A plantar wart (also verruca plantaris or commonly known as verruca) is a wart caused by the human papillomavirus (HPV) occurring on the sole or toes of the foot.

There is currently no cure or treatment for HPV infection. (ZOMG)

It is estimated that 7-10% of the US population is infected. (Wow. Thats like 2.1 million to 3 million people. BROTHERS!) Infection typically occurs on moist walking surfaces such as showers, swimming pools, or shoes. (DAMN. No more swimming) The virus can survive many months without a host, making it highly contagious.

Because plantar warts are spread by contact with moist walking surfaces, they can be prevented by not walking barefoot in public areas such as showers or communal changing rooms, not sharing shoes and socks, and avoiding direct contact with warts on other parts of the body or on other people. (So uhhhh... Don't touch my foot, kaes. Right foot.) Humans build immunity with age, so infection is less common among adults than children. (Seeee uncle. I'm still young. Children.)

Once a person is infected, there is no evidence that any treatment eliminates HPV infection or decreases infectivity, and warts may recur after treatment because of activation of latent virus present in healthy skin adjacent to the lesion. There is currently no vaccine for these types of the virus. However, treatments are sometimes effective at addressing symptoms and causing remission (inactivity) of the virus.

Hahaha. Okay la. I got scared when I read it at first cause I thought this thing was like... no sweat man! So its more serious than I thought eh? Maybe I should tell the ns doctor and get him to de-pes me. hahaha!

Warning! The following is dense, even for bio students

The HPV lifecycle strictly follows the differentiation program of the host keratinocyte. It is thought that the HPV virion infects epithelial tissues through micro-abrasions, whereby the virion associates with putative receptors such as alpha integrins and laminins, leading to entry of the virions into basal epithelial cells through clathrin-mediated endocytosis and/or caveolin-mediated endocytosis depending on the type of HPV. At this point, the viral genome is transported to the nucleus by unknown mechanisms and establishes itself at a copy number between 10-200 viral genomes per cell. A sophisticated transcriptional cascade then occurs as the host keratinocyte begins to divide and become increasingly differentiated in the upper layers of the epithelium. The viral oncogenes, E6 and E7, are thought to modify the cell cycle so as to retain the differentiating host keratinocyte in a state that is amiable to the amplification of viral genome replication and consequent late gene expression. E6 in association with host E6 AP (associated protein), which has ubiquitin ligase activity act to ubiquitinate p53 leading to its proteosomal degradation. E7 (inoncogenic HPV's) acts as the primary transforming protein. E7 competes for pRb binding, freeing the transcription factor E2F to transactivate its targets, thus pushing the cell cycle forwards. All HPV can induce transient proliferation, but only 16 and 18 can immortalise cell intes (in vitro). It has also been shown that HPV 16 and 18 cannot immortalise primary rat cells alone, there needs to be activation of the ras oncogene. In the upper layers of the host epithelium, the late genes L1 and L2 are transcribed/translated and serve as structural proteins which encapsidate (Encapsidation is the process of incorporating a nucleic acid sequence (e.g., a vector, or a viral genome) into a viral particle) the amplified viral genomes. Virions can then be sloughed off in the dead squames of the host epithelium and the viral lifecycle continues.

@.@

Someone get me a panadol. Fast.