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HUMAN PAPILLOMA VIRUS (HPV)

HUMAN PAPILLOMA VIRUS (HPV). By: Nathalia Cruz. What is a Virus?. Exceptionally simple living microbes. Contain a single type of nucleic acid (DNA or RNA) and a protein coat. Obligatory intracellular parasites. Range from 20 to 14.000 nm in length.

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HUMAN PAPILLOMA VIRUS (HPV)

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  1. HUMAN PAPILLOMA VIRUS(HPV) By: Nathalia Cruz

  2. What is a Virus? • Exceptionally simple living microbes. • Contain a single type of nucleic acid (DNA or RNA) and a protein coat. • Obligatory intracellular parasites. • Range from 20 to 14.000 nm in length. • It’s classification is based on type of nucleic acid, strategy for replication, and morphology

  3. HUMAN PAPILLOMA VIRUS • HPV is the virus that causes warts. • More than 100 different kinds, 30-some of this cause genital HPV. • Spread by sexual contact or from mother to baby. • Genital warts appear 6 weeks to 8 months after contact with an HPV infected person.

  4. HPV • The most common sexually transmitted disease worldwide. • Certain types of HPV are linked with cervical cancer. • Divided into 2 subcategories: Genital Warts and Cervical Dysplasia. • Most people do not know they have it. • There are high risk and low risk types of it.

  5. HISTORY • The papillomaviruses are part of the PAPOVAVIRIDAE family of DNA tumor viruses. • First discovered in the early 40’s. • Gained notoriety in the early 80’s when it was discovered that some types of HPV caused cervical cancer.

  6. MORPHOLOGY • Papilloma virus genome is circular covalently closed double stranded DNA of about 8 kbp. • All PV genes are coded in one of the 2 DNA strands utilizing the alternative splicing for the individual expression of each gene. • Papillomavirus expression is characterized by a large array of mRNAs cells coding for different genes. • 55 nm in diameter.

  7. APPEARANCE

  8. MECHANISM OF INFECTION • All PV exhibit extreme specificity for infection on epithelial cells. • The papillomavirus epitheliotrophy resides in the interaction of specific transmission factors with the viral regulatory region LCR. • The infection normally results in hyperproliferation of the host cell and may lead to transformation and immortalization.

  9. GENITAL WARTS • Sometimes called condylomata acuminata. • Are soft, moist or flesh colored, and appear in the genital area within weeks or months after infection. • Sometimes appear in clusters and are either raised or flat, small or large. • Women: appear in the vulva, cervix, vagina and anus. • Men: Can appear on the scrotum or penis.

  10. LIFE CYCLE (HPV-16) • Starts with the infection of the host cell. • The virus DNA is released within the nucleus • Numerous cellular transcription factors interact with the non-coding viral regulatory region (LCR), starting transcription of the two hpv-16 transforming early genes (E6 and E7). • The transforming proteins interact with the cellular antioncogenic regulator p53 disrupting the cell cycle.

  11. LIFE CYCLE

  12. HPV TYPES • Numbered in order of discovery. • 30 HPV types primarily infect the squamous epithelium of the lower anogenital tracts of both males and females. • HPV types 6, 11, 42, 43, or 44 present as papillary condylomas, may also present as flat lesions that may or may not be visible to the unaided eye are part of the “low-risk” HPV types. • Types 16, 18, 31, 33, 35, 45, 51, 52, and 56 are considered “high-risk” types because they have been found in cervical and other lower genital tract cancers.

  13. HPV GENOMIC ORGANIZATION • Three main regions (early, late and the long control region) • (E) resides the transformation and immortalization potential. • (L) Two capsid genes. • (LCR) contains all the cis-regulatory elements.

  14. HOW HPV CAUSES CANCER • HPV DNA integrates into the host genome. • The proteins E6 and E7 are produced from the resultant DNA. • E6 binds and degrades p53 (a tumor suppressor gene). • If the DNA is altered, the cell keeps replicating. The mutation rate of the cell increases. • E7 binds and degrades retinoblastoma (another tumor suppressor gene). • Retinoblastoma normally keeps the cell from growing too fast or responding to growth stimulators. This inhibitory factor is now lost. • without these two mechanisms to slow down cell growth and prevent mutation. . . • Malignant Transformation Occurs.

  15. Genital warts can be treated by a doctor and by different methods. Podofilox gel: A patient-applied treatment for external genital warts. Imiquimod cream: A patient-applied treatment. Chemical treatments (including trichloracetic acid and podophyllin), which must be applied by a trained health care provider to destroy warts. Cryotherapy: Uses liquid nitrogen to freeze off the warts. Laser therapy: Uses a laser beam or intense lights to destroy the warts. Electrosurgery: Uses and electric current to burn off the warts. Surgery: Can cut away the wart in one office visit . Interferon: an antiviral drug, which can be injected directly into warts. HPV TREATMENT

  16. CURE • There is currently no cure for human papillomavirus. • Once an individual is infected, he or she carries the virus for life even if genital warts are removed. • The development of a vaccine against HPV is under way, but is still not available. • If left untreated, some genital warts may regress on their own.

  17. SOURCES • http://cinvestav.mx/genetica/MyFiles/Papillomavirus/PAPepi.html • http://www.life.umd.edu/classroom/bsci424/BSCI223WebSiteFiles/LectureList.htm#LectureList • WWW.STDSERVICES.ON.NET/STD/WARTS • http://www.ashastd.org/stdfaqs/hpv.html • http://www.niaid.nih.gov/factsheets/stdhpv.htm

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