Tika Ghimirey

Herpes Simplex Virus was prevalent as early as ancient Greek. Dr. Anna Wald Greek scholars termed Herpes to mean creep or crawl in reference to the spreading nature of the disease. In 1893 Vidal was the first to recognize the HPV transmission Histopathology studies revealed the multinucleated giant cells associated with herpes virus infection in 20th century. HSV infection was confirmed in 1919. During the 1920s and 30s natural history of HSV was widely studied In 1930 latency (an immune response) of HSV was characterized Herpes antiviral therapy began in the early 1960s

Herpes simplex virus (HSV) is commonly known as HSV-1 & HSV-2. HSV-1 is usually responsible for cold sores (fever blisters) of the lips and mouth. HSV-2 is usually responsible for genital herpes. Both types of the viruses can cause either of the diseases. One out of five adolescents is infected by genital herpes in the United States First outbreak is usually worse than recurring outbreaks

Symptoms of genital herpes

First outbreak occurs in or around the genital area after 2 3 weeks of infection Tingling sensation in the affected area is the first sign Group of red bumps develop into blisters 2 3 weeks later, more blisters rupture and open into painful sores Women may experience vaginal discharge Lesions eventually dry out and heal rapidly leaving no scar

Symptoms of Oral Herpes

Blisters on lips or may also be on tongue Very painful especially in children Blisters eventually rupture as painful sores Increased salivation and foul breath The blisters disappear within 3 14 days Rarely accompanied by difficulties in swallowing, chills, muscle pain or hearing loss

Virulence

Pathogenesis

HSV has a number of genes related to immune invasion Spreads into craniospinal ganglia Establishes latency in the ganglia During latency there is very low or no viral replication

Multiplies in epithelial layer Produces cell destruction and blisters Resides in sensory nervous system Stress related recurrence

HSV is spread by contact like kissing a child or with adults by a virusshedding person. Mainly a disease of children under 5 years old Two peaks of incidences: first from 0 - 5 years and second in the late teens, when sexual activity commences. About 10% population acquire HSV infection through genital route Generally, HSV-1 infects above the belt and HSV-2 infects below it 40% isolation from genital sores is HSV-1 and 5% from facial sores is HSV-2. (Data is complicated due to oral sex practice) The mean number recurrences per year is 1.6

HSV cell culture results are negative in normal condition A cell culture positive for HSV implies probable active infection A negative HSV cell culture does not rule out HSV infection

PREVENTION

TREATMENT

Avoid intimate contact if sores are seen on the body Latex condoms should be used even if no sores Oral sex practice should be stopped If you touch sores, wash your hands with water.

Dormant stage cannot be cured Medication that kills HSV can kill the nerve cells Acute outbreak uses antiviral drugs such as Acyclovir, Valaclovir or Famcyclovir

When you've got HSV, you've got it forever.

Source: CDC

Tika Ghimirey

Human Papilloma Virus (HPV) is a group of DNA (double stranded) viruses.

Causes warts and certain cancers

100+ types have been fully identified.

30 novel types detected - not completely identified. All differ slightly from each other in their genetic structure.

HPV infection is caused by a double stranded DNA virus called human papilloma virus.

Some are related to cervical and

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vaginal cancer and some to lower genital skin warts

HPV rarely causes symptoms Presence of warts in the external genitals may be too small to notice

Bleeding during and after

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intercourse (may occur with cervical cancer)

Irregular vaginal bleeding between periods Abnormal discharge without itching or burning

PATHOGENESIS

VIRULENCE FACTOR

HPV Infection stimulates cellular proliferation (rapid reproduction of cells) in stratified squamous epithelial cells Cells show broad spectrum of changes ranging from benign hyperplasia (enlargement of an organ or tissue) to dysplasia to invasive carcinoma.

Involves proteins E6 & E7 These proteins inactivate hosts tumor suppressor protein p53 & Rb This results in rapid host cell division Produces cancerous cells.

Transmitted through skin to skin contact during sexual intercourse. Exact risk of transmission of genital warts in a single episode of sexual intercourse is unknown Incubation period is 4 weeks to 7 months Remains latent for years in some cases If a partner has certain HPV infection, the other partner will also have the same type of viral infection.

Traditional method of viral diagnosis using electron microscopy is not possible for HPV Cell culture and certain immunological methods is also not suitable The usual method of viral detection is the hybridization of viral nucleic acid by: a. b. polymerase chain reaction and Hybrid Capture of HPV DNA Test 2 (hc2)

PREVENTION

TREATMENT

Vaccines prevent most common HPVs (these vaccines are given with a three shot series) Use condoms Stick to one partner

Trichloroacetic acid Electro-therapy Imiquimod cream (5% cream) Podophylotoxin (0.15% cream)

American Cancer Society. (October 31, 2005) What are the Key Statistics about Cervical Cancer? Detailed Guide: Cervical Cancer. National Institutes of Health (NIH). (1996) NIH Consensus Statement: Cervical Cancer. 14:1-38. Grimshaw, LJ. (2005) How to recognize and manage HPV infections. Kelly, Cowen. Biol 2420 Tarrant County College South Campus. 3rd Boston: McGraw-Hill Companies, 2012. Print. Murphy, Pam.Student presentation on Proteus mirabilis. University November2012<http://web.uconn.edu> of Connecticut Web. 13 Clinical Advisor. 8(3):24-32). ed.