Human papillomavirus, or HPV, is a common group of viruses that can affect various parts of the body. It is a widespread infection, with many individuals acquiring it at some point in their lives, often without realizing it.
Understanding the HPV Virus
HPV is a double-stranded DNA virus belonging to the Papillomaviridae family. Unlike some other viruses, HPV is non-enveloped, meaning it lacks an outer lipid membrane. Its genetic material, a circular double-stranded DNA genome, is protected by a protein shell known as a capsid.
The capsid is constructed from two viral proteins: the major capsid protein L1 and the minor capsid protein L2. Over 200 different types of HPV have been identified, with more than 40 types known to infect the anogenital area.
These HPV types are categorized into low-risk and high-risk groups based on their health implications. Low-risk types, such as HPV 6 and 11, are associated with genital warts and are generally not linked to cancer. High-risk types, including HPV 16 and 18, can cause cellular changes that may progress to certain cancers.
How HPV Replicates in Cells
The HPV infection process begins when the virus enters the basal cells of the epithelium, typically through minor abrasions or breaks in the skin. Once inside, the viral DNA genome is transported to the host cell’s nucleus. The life cycle of HPV is closely intertwined with the differentiation program of the infected epithelial cells.
In the initial phase, referred to as establishment replication, the incoming viral genome undergoes limited amplification. This leads to approximately 10 to 50 viral DNA copies within each infected cell. This early replication step relies on viral proteins E1 and E2, which recruit the host cell’s own DNA replication machinery.
Following establishment, the virus enters a maintenance phase within actively dividing basal cells. During this stage, the viral DNA replicates in synchrony with the host cell’s DNA, ensuring a stable copy number is passed to daughter cells. As infected cells undergo differentiation and migrate towards the upper layers of the epithelium, the virus initiates vegetative replication.
Vegetative replication involves a significant increase in viral genome copies, often reaching hundreds or thousands per cell. The viral oncoproteins E6 and E7, particularly from high-risk HPV types, facilitate this process by influencing host cell cycles and promoting proliferation, thereby supporting extensive viral replication. In the later stages of the viral life cycle, within terminally differentiated cells, the L1 and L2 capsid proteins are produced. These proteins assemble in the nucleus, encapsidating the newly replicated viral DNA genomes to form new infectious viral particles. The release of these new virions occurs as the infected, terminally differentiated cells are shed from the skin surface.
Transmission Pathways of HPV
HPV is highly contagious, primarily transmitting through direct skin-to-skin contact. For genital HPV infections, sexual activity is the most frequent route of spread.
This includes various forms of sexual contact, such as vaginal, anal, and oral sex. Transmission can occur through direct contact between genital areas, or between oral and genital or anal areas. Penetrative sex is not a requirement for HPV transmission; any intimate skin contact can facilitate its spread. The virus can also be transmitted even when an infected individual shows no visible symptoms.
Less common pathways of transmission include hand-to-genital contact. In rare instances, vertical transmission from a pregnant individual to their baby during childbirth is also possible. Direct skin contact remains the most common and established mechanism for HPV spread. The virus does not transmit through bodily fluids such as blood or semen.