Understanding HPV: A Comprehensive Overview.pptx

The "HPV" PowerPoint presentation offers a comprehensive overview of human papillomavirus (HPV). Key aspects include:

Introduction and Structure:

HPV is a small, non-enveloped DNA virus with an icosahedral capsid.
Replication Strategy:

Details the replication process in epithelial cells, from entry to the release of new virions.
Pathogenesis:

Discusses transmission, entry into the host, replication, and clinical manifestations like genital warts and cancer.
Epidemiology:

HPV is the most common sexually transmitted infection globally, especially in young adults aged 15-24 years, and prevalent in lower-income countries.
Clinical Presentation:

Includes cutaneous warts, head and neck tumors, genital warts, and cancer.
Complications:

Severe outcomes like cervical cancer and respiratory papillomatosis are covered.
Immune Response:

Describes innate and adaptive immune responses, including cytotoxic T cells and memory response.
Diagnosis:

Methods include colposcopy, acetic acid test, biopsy, DNA tests (PCR, hybridization), and Pap smears.
Treatment and Prevention:

Treatment options for warts and preventive measures like safe sexual practices are discussed.
This presentation provides essential information on HPV, its health impacts, and management and prevention strategies

1. hpv Introduction Papillomaviruses are small, non-enveloped, icosahedral DNA viruses that have a diameter of 52–55 nm. The viral particles consist of a single double-stranded DNA molecule of about 8000 base-pairs (bp) that is bound to cellular histones and contained in a protein capsid composed of 72 pentameric capsomers.

2. Viral replication strategy Human papillomavirus (HPV) replicates primarily in epithelial cells. The replication process involves several steps: 1. Attachment and Entry: HPV initially attaches to epithelial cells via interactions between viral capsid proteins and cell surface receptors. The virus enters the cell through endocytosis. 2. Uncoating and Genome Release : Once inside the cell, the viral capsid undergoes disassembly, releasing the viral genome into the cytoplasm. 3. Transcription and Translation: The viral genome is a double-stranded DNA molecule. Viral gene expression occurs in a regulated cascade. 4. Replication : HPV DNA replication takes place in the nucleus of infected cells. The viral DNA replicates using host cell DNA polymerases and other cellular machinery 5. Assembly and Release: Late in the viral life cycle, viral capsid proteins are synthesized and assembled into new virions in the nucleus. Mature virions are released from the infected cell, often through cell lysis or exocytosis, to infect neighboring cells.

3. Viral replication strategy

4. Pathogenesis of disease 1. Transmission: HPV is primarily transmitted through direct skin-to-skin contact, including sexual contact. 2. Entry into the host: The virus enters the body through micro-abrasions or epithelial disruptions in the skin or mucous membranes especially anogenital. 3. Attachment and entry into epithelial cells : infects the basal cells of the stratified squamous epithelium. The virus attaches to receptors on the basal cells' surface and enters the cells through endocytosis. 4. Viral genome replication: Once inside , the viral genome is released and transported to the nucleus. The viral DNA replicates along with the host cell DNA, utilizing the host cell's machinery for replication.

5. Pathogenesis of disease

6. Pathogenesis of disease 5. Viral gene expression and protein synthesis : HPV gene expression occurs in a regulated manner to evade host immune responses and facilitate viral replication. 6. Cell cycle dysregulation and immune evasion : HPV-encoded oncoproteins (E6 and E7) interfere with host cell cycle regulation and apoptosis, promoting cell proliferation and inhibiting cell death. This dysregulation contributes to the development of HPV . 7. Development of clinical manifestations : HPV infections can manifest in various ways, genital warts (low-risk HPV types) , precancerous and cancerous lesions (high-risk HPV types). Persistent infection with high-risk HPV types can lead to the development of cancer

7. Epidemiology Human papilloma virus (HPV) is the most sexually transmitted infection globally. HPV infection is most common among young adults who are sexually active aged 15 -24 years due to high hormonal levels. It is most in lower Income countries for example Zambia which is a developing country, unlike high countries which have higher vaccination coverage rate.

8. Clinical presentation Human papilloma virus infection causes: (a) Cutaneous warts, (b) Benign head and neck tumors, (c) Genital warts, (d) Cancerous conditions in humans .

9. Clinical presentation CUTANEOUS WARTS: These are commonly caused by HPV-2, HPV-4 , and HPV-7. Warts usually develop on the hands and feet after incubation period of 34 months depending on the HPV type and the site of infection. They may appear flat, plantar, or dome shaped. The plantar and flat warts are most common in children and young adults. Wart is usually a benign and self-limiting condition, which resolves during the course of time .

10. Clinical presentation BENIGN TUMORS OF HEAD AND NECK: These include oral papilloma, laryngeal papilloma, and conjunctival papilloma. Oral papillomas are usually single but may be multiple. They are sessile, verrucous, and white with raised borders. These lesions usually appear on the lips, hard palate, or gingiva. Focal epithelial hyperplasia or Heck disease is commonly caused by HPV-13 and HPV-32. This condition manifests as multiple, smooth, and sessile nodules present on the mucosal surface of the lower lip or on the buccal mucosa. This condition was described in North American people. Laryngeal papillomas are life-threatening conditions in children, caused by HPV-6 and HPV-11. This is the most common benign epithelial tumor of the larynx.

11. Clinical presentation GENITAL WARTS OR CONDYLOMA ACUMINATA : Caused by HPV-6 and HPV-11. The condition typically manifests as solitary or multiple cerebriform and pink lesions, which appear more commonly on the nonkeratinized mucosa than on the keratinized mucosa. These genital lesions may also spread to the oral cavity during sexual activity involving orogenital contact.

12. Clinical presentation CANCEROUS CONDITIONS: Certain types of HPV commonly, HPV16 and less frequently, HPV18, HPV33, HPV35 have been associated with oral premalignancy and malignancies in humans. These conditions are associated with verruciform proliferations in the oral cavity. Oral premalignant lesions and oral squamous cell carcinoma caused by HPV16 and HPV18 are most commonly associated with intraepithelial cervical neoplasia and cancer. The conditions progresses from mild to moderate neoplasia to severe dysplasia or carcinoma in situ during a period of 14 years

13. Complication of this infection 1.Cervical Cancer: Persistent infection with high-risk HPV types, particularly HPV 16 and 18, is the primary cause of cervical cancer. According to the World Health Organization (WHO), cervical cancer is the fourth most common cancer in women globally. 2.Genital Warts: HPV infection with low-risk types, such as HPV 6 and 11, can cause genital warts. These warts can appear on the genitals, in the anal area, or in the mouth and throat. While not typically cancerous, they can cause discomfort and psychological distress. 3.Respiratory Papillomatosis: This is a rare condition where warts caused by HPV grow in the throat, voice box, or lungs. It can lead to breathing problems, voice changes, and in severe cases, respiratory obstruction.

14. Complication of this infection 4.Recurrent Respiratory Papillomatosis (RR P): This condition is characterized by the recurrent growth of benign tumors in the respiratory tract, particularly in the larynx. It is caused by HPV types 6 and 11 and primarily affects children. 5.Pregnancy Complications: HPV infection during pregnancy can lead to complications such as genital warts, which may increase the risk of cesarean delivery. In rare cases, transmission of HPV to the newborn during delivery can lead to respiratory papillomatosis. 6.Psychosocial Impact: Living with HPV infection, especially if it leads to visible symptoms like genital warts, can have a significant psychosocial impact. It may cause anxiety, depression, relationship issues, and stigma

15. Host immune response The exact mechanism responsible for resolution of papillomas is said to be cell mediated. If Patient is immunocompromised (HIV / Immunosuppressive therapy) this can result in a severe manifestation of the disease. The host immune response to HPV involves both innate and adaptive immunity. 1. Innate Immune Response: Upon infection with HPV, the innate immune system is activated. Cells such as dendritic cells and macrophages recognize the presence of the virus and initiate a release of cytokines and chemokines to recruit other immune cells to the site of infection thus creating a pro-inflammatory microenvironment to eliminate the infected cells, initiating an effective acquired immune response.

16. Host immune response 2. Adaptive Immune Response: The adaptive immune response involves the activation of T cells and B cells. Cytotoxic T cells (CD8+) recognize and kill cells infected with HPV, preventing the spread of the virus. Helper T cells (CD4+) stimulate B cells to produce antibodies against HPV 3.Memory Response: After the initial infection, the immune system retains a memory of the virus. This memory response allows for a faster and more effective immune reaction upon subsequent exposures to the virus. Vaccines against HPV are designed to stimulate the immune system to produce a memory response without causing the disease.

17. Laboratory diagnosis The laboratory diagnosis of papilloma virus typically involves several important methods and these are: Colposcopy: This is the examination of the cervix, vagina and in some instances the vulva after the application of acetic acid solution. Colposcopy allows illuminated stereoscopic and magnified viewing of the cervix. It is used to find cancerous cells or abnormal cells that can become cancerous in the cervix, vagina or vulva. Acetic acid test: When demonstrating this test, a vinegar solution is applied to HPV- infected areas which turn white. This may help in identifying difficult to see flat lesions. Biopsy: A sample of tissue is taken from the cervix, vagina or vulva and taken for examination under a microscope. If the biopsy results show pre-cancer(dysplasia) or cancer, then treatment is recommended. The dysplasia my be mild, moderate or severe.

18. Laboratory diagnosis 4. DNA test(PCR, DNA hybridization): PCR is a highly sensitive and specific technique used to detect HPV DNA in clinical samples such as cervical swabs, tissue biopsies, or warts. It amplifies specific DNA sequences of the virus for detection.DNA Hybridization uses specific probes that bind to HPV DNA sequences. If HPV DNA is present in the sample, it will hybridize with the probes, indicating the presence of the virus. 5. Pap smear ( pap test): Pap smear is a screening method. It involves collecting cells from the cervix and examining them under a microscope for abnormalities, including those caused by HPV infection.

19. Treatment Medications to eliminate warts are typically applied directly to the lesion and usually take many applications before they're successful. Salicylic acid Surgical and other procedures Freezing with liquid nitrogen (cryotherapy) Burning with an electrical current (electrocautery) Surgical removal Laser surgery

20. Prevention No specific preventive measures are available against HPV infection. Avoidance of direct contact with infected warts may prevent transmission. Safe sexual practice will be useful to prevent sexual transmission of HPV-Abstain from sexual intercourse.

21. References "Fields Virology" by David M. Knipe et al. (Book) World Health Organization (WHO) - https://www.who.int/health-topics/cervical-cancer Centers for Disease Control and Prevention (CDC) - https://www.cdc.gov/hpv/index.html American Cancer Society - https://www.cancer.org/cancer/cancer-causes/infectious-agents/hpv.html https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6688195/ Textbook of Microbiology & Immunology 2 nd Edition by Subhash Chandra Parija