{"id":4840,"date":"2025-10-17T18:32:58","date_gmt":"2025-10-17T22:32:58","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=4840"},"modified":"2026-01-03T16:16:56","modified_gmt":"2026-01-03T21:16:56","slug":"human-papilloma-virus-patient-medical-education-pamphlet-student-activity","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/human-papilloma-virus-patient-medical-education-pamphlet-student-activity\/","title":{"raw":"Human Papilloma Virus - Patient Medical Education Pamphlet - Student Activity","rendered":"Human Papilloma Virus – Patient Medical Education Pamphlet – Student Activity"},"content":{"raw":"

Background Information: <\/strong><\/h1>\r\nHuman Papilloma Virus is responsible for causing epithelial lesions (e.g., warts) and some epithelial cancers.\u00a0 There are over 100 subtypes of HPV, some of which can cause 3 different types of lesions: non-genital (cutaneous) lesions, mucosal or genital lesions, and various epithelial cancers (e.g., cervical cancer, and some laryngeal, oral, lung, penile, and anogenital cancers).\u00a0 Usually, HPV infection alone doesn\u2019t cause cancer, but with multiple factors combined (e.g., smoking, UV light exposure, immunosuppression, pregnancy and\/or repeated HPV infections).\u00a0 HPV infects the skin and enters the basal stem cells of the epidermis.\u00a0 As HPV can be sexually transmitted, multiple sexual partners increasing one\u2019s risk for the HPV genital infections.\u00a0 HPV infections on other parts of the body (e.g., feet) can occur through contact with the virus in rec centre change room facilities.\u00a0 In the USA, it is estimated that 45.2% of males and 39.9% of females (aged 18-59) are infected with genital HPV. \u00a0In total, more than 42 million Americans are currently infected with HPV and 13 million Americans become infected each year.\u00a0 Stats in Canada are likely similar.\r\n\r\nSome subtypes of HPV are oncoviruses and lead to DNA mutations in basal epidermal stem cells that transform the cells into immortal cancerous cells.\u00a0 Cervical Pap smears are available for females and anal Pap smears are available for males.\u00a0 Although many cases of HPV infection are asymptomatic, signs & symptoms of HPV anogenital infections include: bleeding, pelvic\/genital pain, and\/or palpable lesions.\u00a0 Pap smears can reveal dysplasia and concurrent HPV testing can indicate the need for follow-up tests, which can include colposcopy and targeted biopsies and DNA testing.\u00a0 Treatments of cutaneous & anogenital warts can involve surgical removal, cryotherapy, and laser removal.\u00a0 Further treatment (e.g., chemotherapy and\/or radiation) may be required if transformation to malignant cancer has occurred.\u00a0 Prevention of anogenital HPV infections involves vaccination prior to HPV infections, often given at 11-12 yrs old. \u00a0Other means of prevention include use of barriers (e.g., condoms) during sexual intercourse, though this is not 100% preventative as it doesn\u2019t eliminate all skin-skin contact. \u00a0Treatment of sore arms and mild fever that sometimes occurs during vaccination involves the use of acetaminophen and\/or ibuprofen.\u00a0 ASA (aspirin) is typically not given, especially to those under the age of 18 due to the risk of developing Reye syndrome.\r\n\r\n \r\n

Word Bank: Possible Lesson 1&2 Terms:<\/strong><\/h1>\r\npathogen, exogenous, endogenous, morbidity, mortality, epidemic, endemic, pandemic, communicable, latent, subclinical, acute, chronic, lesion, neglected tropical disease, atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, anaplasia, neoplasia, immature, dedifferentiate, dysfunctional, non-functional, proliferation\/mitosis, true\/false negative test results, true\/false positive test results, sensitive test, specific test, redness, warmth, swelling, exudate, pain, histamine, bradykinin, prostaglandin, capillary permeability, vasodilation, chemokines, lymphokine, diapedesis\/emigration\/transmigration, chemotaxis, inflammatory cytokines, C reactive protein, (erythrocyte sedimentation rate, ESR), neutrophils, basophils, mast cells, eosinophils, macrophages, dendritic cells, Helper T cells, Cytotoxic T cells, Memory B cells, Plasma Cells, Antibodies, Opsonization, Interferons, Anti-Viral Proteins (AVPs), free radicals, Reactive Oxidative Species, (ROS), phagocytosis, pyrexia, Memory Helper T cells, Memory Cytotoxic T cells, Suppressor T cells, NK lymphocytes, Primary & Secondary Response.\r\n\r\n \r\n

Title:<\/strong>\u00a0 Human Papilloma Virus Infections - Information Sheet\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Team-Lead Name:<\/strong> ____________________<\/h1>\r\n

Etiology<\/strong>:<\/h1>\r\nHuman Papillomavirus infection, HPV is a non-enveloped, double-stranded, circular DNA virus\r\n

Risk Factors<\/strong>:<\/h1>\r\nsexual activity, number of sexual partners (as increases likelihood of contact with oncovirus strains of HPV), transmitted through skin-to-skin contact\r\n

Prevalence & Incidence<\/strong>:<\/h1>\r\nthe most common STD worldwide, ~50% of sexually active adults\r\n

Pathogenesis<\/strong><\/h1>\r\n(List the steps of cellular & morphological changes that occur if infected with HPV oncovirus):\r\n
    \r\n \t
  1. HPV infects basal keratinocytes (epithelial cells) of the epidermis of skin or mucosal surface.<\/li>\r\n \t
  2. HPV can produce epithelial benign\/malignant tumors of the skin and mucous membranes.<\/li>\r\n \t
  3. Some strains (subtypes) of HPV cause DNA mutation when they integrate their genome into the host DNA. Co-factors such as tobacco use, UV radiation (and other carcinogens), pregnancy, folate deficiency, immune suppression, female oral contraceptive use, pregnancy increase the risk of cancer-causing DNA mutations occurring.<\/li>\r\n \t
  4. Specifically, once inside basal epithelial cells, cancer-causing HPV strains\/subtypes produce 2 viral proteins (oncoproteins that inactivate stability proteins (p53 and pRb) that can lead to DNA errors during DNA duplication during mitosis. Other carcinogens (e.g., tobacco) can lead to more DNA mutations.\u00a0 These DNA mutations can give rise to hypertrophic lesions (e.g., warts) and possibly dysplasia and anaplasia (unregulated and continuous mitosis, immortality = cell becomes cancerous).<\/li>\r\n \t
  5. Summary: HPV infection can give rise to genital and non-genital warts, lesions, and cancers (e.g., cervical cancer, anal cancer).\u00a0 Non-cancerous genital warts can regress spontaneously or with treatment (see below). Cancers require treatment (see below)<\/li>\r\n<\/ol>\r\n

    Steps of Inflammatory Response:\u00a0\u00a0\u00a0 <\/strong><\/h1>\r\n
      \r\n \t
    1. Cellular damage (the release of cellular contents) as well as presence of foreign material (e.g., viral\/bacterial\/fungal) triggers the release of vasoactive cytokines (e.g., histamine, leukotrienes, prostaglandins, bradykinins) from Mast Cells and Basophils. These vasoactive cytokines:<\/li>\r\n \t
    2. Bind to blood vessel walls inducing vasodilation and increased capillary permeability. The resulting increase in blood flow causes Redness<\/strong> and Warmth.<\/strong> The exudate leaking from the capillaries causes Swelling.<\/strong>\u00a0 Pain<\/strong> is caused by nociceptors (pain-relaying sensory neurons) being triggered by: a) the pressure from the leaking exudate; b) chemicals released during cellular damage; c) prostaglandins and d) leaked blood.<\/li>\r\n \t
    3. Mast cells and Basophils also release cytokines and chemokines that attract WBCs to the area to assist with eliminating any infection and removing cellular debris. Platelets are activated to wall off the area of damage. WBCs and surrounding epithelial and connective tissue cells release growth factors to stimulate mitosis, regeneration, and replacement of dead cells.\u00a0 Cells that can not be replaced through regeneration lead to more collagen being laid down which contributes to scarring (fibrosis).<\/li>\r\n<\/ol>\r\n

      Differences in mechanism between aspirin, ibuprofen, acetaminophen, and corticosteroids:<\/strong><\/h1>\r\n
        \r\n \t
      1. Acetylsalicylic acid (ASA): eg. Aspirin\r\nBlocks COX-1\/2 \u2192 \u2193 production of PGs reducing inflammation, pain, & fever;\r\nNot to be used during viral infection \u2192 Reye\u2019s syndrome (liver & brain damage)\r\nCan be an allergen; Can \u2193 gastric mucus \u2192 can cause stomach irritation & ulcers\r\nCan interfere with blood clotting (reduces platelet adhesion)<\/li>\r\n \t
      2. Acetaminophen (e.g. Tylenol)\r\nBlocks COX-2 \u2192\u2193production of PG E2 \u2192 \u2193fever & pain , but not inflammation<\/li>\r\n \t
      3. Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. Ibuprofen, Advil, Motrin - also works by blocking COX-1\/2 \u2192 \u2193 production of PGs\r\nDecrease fever, pain & inflammation; with less negative side-effects of aspirin<\/li>\r\n \t
      4. Glucocorticoids (steroidal anti-inflammatory drugs) e.g. Corticosteroids\r\nDecreases: capillary permeability (limits emigration\/chemotaxis), # of WBCs, # mast cells, release of histamine, prostaglandins & leukotrienes\r\nNegative side-effects: lymphoid tissue atrophy (decreased # WBCs leading to risk of infection & reduced immune response); catabolism; thinning skin (peptic ulcers), delayed healing, delayed growth, high bp & edema (Na and H2O retention).<\/li>\r\n \t
      5. Catabolism:\u00a0 protein \u2192 amino acid \u2192 glucose (gluconeogenesis)<\/li>\r\n \t
      6. Diagnostic Tools<\/strong>:\u00a0 Sensitive test = Pap Test (cytologic testing), DNA testing, clinical analysis of lesions and warts (exhibiting hyperkeratosis and hyperplasia); if Pap Test is positive = Specific Test = colposcopy<\/li>\r\n<\/ol>\r\n

        Treatment<\/strong>:<\/h1>\r\n
          \r\n \t
        1. For non-dysplastic and non-cancers: Cryosurgery\/electrosurgery\/scalpel excision\/laser ablation of warts, immune response modifiers for anogenital warts, cytotoxic agents for nongenital warts<\/li>\r\n \t
        2. For dysplasia<\/li>\r\n \t
        3. For cancers: surgery\/chemotherapy\/radiation depending on stage\/grade (spread and cellular characteristics) of cancer<\/li>\r\n<\/ol>\r\n

          Potential Complications<\/strong>:<\/h1>\r\nnon-genital and genital warts, cervical dysplasia and\/or cervical cancer, vaginal cancer, penile cancer, throat cancer, anal cancer\r\n

          Prevention<\/strong>:<\/h1>\r\ncondoms, HPV vaccine (prior to sexual activity)\r\n

          Vaccine Mechanism (mode of action)<\/strong><\/h1>\r\nList Cellular Steps of WBC Response:\r\n
            \r\n \t
          1. Injection of 14 HPV viral proteins from oncovirus strains to initiate Primary Response of the Specific Immune system (activation of B and T cells) as follows:<\/li>\r\n \t
          2. Phagocytosis of viral proteins by phagocytes such as macrophages, dendritic cells, and B lymphocytes (B cells) which will become Antigen Presenting Cells (APCs).<\/li>\r\n \t
          3. Activation of Helper T lymphocytes (i.e. TH<\/sub> cells, CD4 cells)<\/strong> and Cytotoxic T lymphocytes (i.e., Tc cells, Killer T cells, CD8 cells)<\/strong>,\u00a0 through APC display of viral antigens on Class II MHCs and APC release of lymphokines (e.g., monokines and interleukins).<\/li>\r\n \t
          4. Helper and Cytotoxic T lymphocytes with T cell receptors (TCRs)<\/strong> that match\/bind to the viral antigen being presented will proliferate producing daughter TH<\/sub> cells, daughter Memory\u00a0TH <\/sub>cells, daughter TC<\/sub> cells, daughter TC<\/sub>\u00a0 Memory cells, daughter TR<\/sub> Regulatory cells.<\/li>\r\n \t
          5. TH<\/sub> cells are instrumental in activating TC<\/sub> cells and do so by binding viral antigen to TCR and releasing lymphokines.<\/li>\r\n \t
          6. Active TC<\/sub> cells go on a search and destroy (seek and destroy mission) mission to destroy HPV viral antigens. Memory T cells allow for prolonged memory and faster response times during Secondary Response.<\/li>\r\n \t
          7. Activation of B lymphocytes begin with viral antigen binding to their IgD receptors and intake\/phagocytosis of viral proteins \u2013 to become sensitized. Then, B cells display viral proteins on Class II MHCs and bind to Helper T cells that have also been activated (by their TCR binding to viral proteins).<\/li>\r\n \t
          8. Once activated B cells proliferate and their daughter plasma cells produce antibodies against HPV.\u00a0 Their other daughter cells are Memory B cells.<\/li>\r\n \t
          9. Antibodies travel the bloodstream (and other regions) to bind viral antigen, targeting it for destruction.<\/li>\r\n \t
          10. Regulatory T cells will de-activate the B and T cell response once the viral antigen or infection has been eliminated.<\/li>\r\n \t
          11. The build up of Memory B, Memory TH<\/sub> cells, and Memory T<\/span>C<\/sub> cells allows for a very rapid (secondary) response the next time the person is exposed to HPV, meaning that it can eliminate the virus before it has a chance to enter cells and cause cancer.<\/span><\/li>\r\n<\/ol>","rendered":"

            Background Information: <\/strong><\/h1>\n

            Human Papilloma Virus is responsible for causing epithelial lesions (e.g., warts) and some epithelial cancers.\u00a0 There are over 100 subtypes of HPV, some of which can cause 3 different types of lesions: non-genital (cutaneous) lesions, mucosal or genital lesions, and various epithelial cancers (e.g., cervical cancer, and some laryngeal, oral, lung, penile, and anogenital cancers).\u00a0 Usually, HPV infection alone doesn\u2019t cause cancer, but with multiple factors combined (e.g., smoking, UV light exposure, immunosuppression, pregnancy and\/or repeated HPV infections).\u00a0 HPV infects the skin and enters the basal stem cells of the epidermis.\u00a0 As HPV can be sexually transmitted, multiple sexual partners increasing one\u2019s risk for the HPV genital infections.\u00a0 HPV infections on other parts of the body (e.g., feet) can occur through contact with the virus in rec centre change room facilities.\u00a0 In the USA, it is estimated that 45.2% of males and 39.9% of females (aged 18-59) are infected with genital HPV. \u00a0In total, more than 42 million Americans are currently infected with HPV and 13 million Americans become infected each year.\u00a0 Stats in Canada are likely similar.<\/p>\n

            Some subtypes of HPV are oncoviruses and lead to DNA mutations in basal epidermal stem cells that transform the cells into immortal cancerous cells.\u00a0 Cervical Pap smears are available for females and anal Pap smears are available for males.\u00a0 Although many cases of HPV infection are asymptomatic, signs & symptoms of HPV anogenital infections include: bleeding, pelvic\/genital pain, and\/or palpable lesions.\u00a0 Pap smears can reveal dysplasia and concurrent HPV testing can indicate the need for follow-up tests, which can include colposcopy and targeted biopsies and DNA testing.\u00a0 Treatments of cutaneous & anogenital warts can involve surgical removal, cryotherapy, and laser removal.\u00a0 Further treatment (e.g., chemotherapy and\/or radiation) may be required if transformation to malignant cancer has occurred.\u00a0 Prevention of anogenital HPV infections involves vaccination prior to HPV infections, often given at 11-12 yrs old. \u00a0Other means of prevention include use of barriers (e.g., condoms) during sexual intercourse, though this is not 100% preventative as it doesn\u2019t eliminate all skin-skin contact. \u00a0Treatment of sore arms and mild fever that sometimes occurs during vaccination involves the use of acetaminophen and\/or ibuprofen.\u00a0 ASA (aspirin) is typically not given, especially to those under the age of 18 due to the risk of developing Reye syndrome.<\/p>\n

             <\/p>\n

            Word Bank: Possible Lesson 1&2 Terms:<\/strong><\/h1>\n

            pathogen, exogenous, endogenous, morbidity, mortality, epidemic, endemic, pandemic, communicable, latent, subclinical, acute, chronic, lesion, neglected tropical disease, atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, anaplasia, neoplasia, immature, dedifferentiate, dysfunctional, non-functional, proliferation\/mitosis, true\/false negative test results, true\/false positive test results, sensitive test, specific test, redness, warmth, swelling, exudate, pain, histamine, bradykinin, prostaglandin, capillary permeability, vasodilation, chemokines, lymphokine, diapedesis\/emigration\/transmigration, chemotaxis, inflammatory cytokines, C reactive protein, (erythrocyte sedimentation rate, ESR), neutrophils, basophils, mast cells, eosinophils, macrophages, dendritic cells, Helper T cells, Cytotoxic T cells, Memory B cells, Plasma Cells, Antibodies, Opsonization, Interferons, Anti-Viral Proteins (AVPs), free radicals, Reactive Oxidative Species, (ROS), phagocytosis, pyrexia, Memory Helper T cells, Memory Cytotoxic T cells, Suppressor T cells, NK lymphocytes, Primary & Secondary Response.<\/p>\n

             <\/p>\n

            Title:<\/strong>\u00a0 Human Papilloma Virus Infections – Information Sheet\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Team-Lead Name:<\/strong> ____________________<\/h1>\n

            Etiology<\/strong>:<\/h1>\n

            Human Papillomavirus infection, HPV is a non-enveloped, double-stranded, circular DNA virus<\/p>\n

            Risk Factors<\/strong>:<\/h1>\n

            sexual activity, number of sexual partners (as increases likelihood of contact with oncovirus strains of HPV), transmitted through skin-to-skin contact<\/p>\n

            Prevalence & Incidence<\/strong>:<\/h1>\n

            the most common STD worldwide, ~50% of sexually active adults<\/p>\n

            Pathogenesis<\/strong><\/h1>\n

            (List the steps of cellular & morphological changes that occur if infected with HPV oncovirus):<\/p>\n

              \n
            1. HPV infects basal keratinocytes (epithelial cells) of the epidermis of skin or mucosal surface.<\/li>\n
            2. HPV can produce epithelial benign\/malignant tumors of the skin and mucous membranes.<\/li>\n
            3. Some strains (subtypes) of HPV cause DNA mutation when they integrate their genome into the host DNA. Co-factors such as tobacco use, UV radiation (and other carcinogens), pregnancy, folate deficiency, immune suppression, female oral contraceptive use, pregnancy increase the risk of cancer-causing DNA mutations occurring.<\/li>\n
            4. Specifically, once inside basal epithelial cells, cancer-causing HPV strains\/subtypes produce 2 viral proteins (oncoproteins that inactivate stability proteins (p53 and pRb) that can lead to DNA errors during DNA duplication during mitosis. Other carcinogens (e.g., tobacco) can lead to more DNA mutations.\u00a0 These DNA mutations can give rise to hypertrophic lesions (e.g., warts) and possibly dysplasia and anaplasia (unregulated and continuous mitosis, immortality = cell becomes cancerous).<\/li>\n
            5. Summary: HPV infection can give rise to genital and non-genital warts, lesions, and cancers (e.g., cervical cancer, anal cancer).\u00a0 Non-cancerous genital warts can regress spontaneously or with treatment (see below). Cancers require treatment (see below)<\/li>\n<\/ol>\n

              Steps of Inflammatory Response:\u00a0\u00a0\u00a0 <\/strong><\/h1>\n
                \n
              1. Cellular damage (the release of cellular contents) as well as presence of foreign material (e.g., viral\/bacterial\/fungal) triggers the release of vasoactive cytokines (e.g., histamine, leukotrienes, prostaglandins, bradykinins) from Mast Cells and Basophils. These vasoactive cytokines:<\/li>\n
              2. Bind to blood vessel walls inducing vasodilation and increased capillary permeability. The resulting increase in blood flow causes Redness<\/strong> and Warmth.<\/strong> The exudate leaking from the capillaries causes Swelling.<\/strong>\u00a0 Pain<\/strong> is caused by nociceptors (pain-relaying sensory neurons) being triggered by: a) the pressure from the leaking exudate; b) chemicals released during cellular damage; c) prostaglandins and d) leaked blood.<\/li>\n
              3. Mast cells and Basophils also release cytokines and chemokines that attract WBCs to the area to assist with eliminating any infection and removing cellular debris. Platelets are activated to wall off the area of damage. WBCs and surrounding epithelial and connective tissue cells release growth factors to stimulate mitosis, regeneration, and replacement of dead cells.\u00a0 Cells that can not be replaced through regeneration lead to more collagen being laid down which contributes to scarring (fibrosis).<\/li>\n<\/ol>\n

                Differences in mechanism between aspirin, ibuprofen, acetaminophen, and corticosteroids:<\/strong><\/h1>\n
                  \n
                1. Acetylsalicylic acid (ASA): eg. Aspirin
                  \nBlocks COX-1\/2 \u2192 \u2193 production of PGs reducing inflammation, pain, & fever;
                  \nNot to be used during viral infection \u2192 Reye\u2019s syndrome (liver & brain damage)
                  \nCan be an allergen; Can \u2193 gastric mucus \u2192 can cause stomach irritation & ulcers
                  \nCan interfere with blood clotting (reduces platelet adhesion)<\/li>\n
                2. Acetaminophen (e.g. Tylenol)
                  \nBlocks COX-2 \u2192\u2193production of PG E2 \u2192 \u2193fever & pain , but not inflammation<\/li>\n
                3. Non-steroidal anti-inflammatory drugs (NSAIDs) e.g. Ibuprofen, Advil, Motrin – also works by blocking COX-1\/2 \u2192 \u2193 production of PGs
                  \nDecrease fever, pain & inflammation; with less negative side-effects of aspirin<\/li>\n
                4. Glucocorticoids (steroidal anti-inflammatory drugs) e.g. Corticosteroids
                  \nDecreases: capillary permeability (limits emigration\/chemotaxis), # of WBCs, # mast cells, release of histamine, prostaglandins & leukotrienes
                  \nNegative side-effects: lymphoid tissue atrophy (decreased # WBCs leading to risk of infection & reduced immune response); catabolism; thinning skin (peptic ulcers), delayed healing, delayed growth, high bp & edema (Na and H2O retention).<\/li>\n
                5. Catabolism:\u00a0 protein \u2192 amino acid \u2192 glucose (gluconeogenesis)<\/li>\n
                6. Diagnostic Tools<\/strong>:\u00a0 Sensitive test = Pap Test (cytologic testing), DNA testing, clinical analysis of lesions and warts (exhibiting hyperkeratosis and hyperplasia); if Pap Test is positive = Specific Test = colposcopy<\/li>\n<\/ol>\n

                  Treatment<\/strong>:<\/h1>\n
                    \n
                  1. For non-dysplastic and non-cancers: Cryosurgery\/electrosurgery\/scalpel excision\/laser ablation of warts, immune response modifiers for anogenital warts, cytotoxic agents for nongenital warts<\/li>\n
                  2. For dysplasia<\/li>\n
                  3. For cancers: surgery\/chemotherapy\/radiation depending on stage\/grade (spread and cellular characteristics) of cancer<\/li>\n<\/ol>\n

                    Potential Complications<\/strong>:<\/h1>\n

                    non-genital and genital warts, cervical dysplasia and\/or cervical cancer, vaginal cancer, penile cancer, throat cancer, anal cancer<\/p>\n

                    Prevention<\/strong>:<\/h1>\n

                    condoms, HPV vaccine (prior to sexual activity)<\/p>\n

                    Vaccine Mechanism (mode of action)<\/strong><\/h1>\n

                    List Cellular Steps of WBC Response:<\/p>\n

                      \n
                    1. Injection of 14 HPV viral proteins from oncovirus strains to initiate Primary Response of the Specific Immune system (activation of B and T cells) as follows:<\/li>\n
                    2. Phagocytosis of viral proteins by phagocytes such as macrophages, dendritic cells, and B lymphocytes (B cells) which will become Antigen Presenting Cells (APCs).<\/li>\n
                    3. Activation of Helper T lymphocytes (i.e. TH<\/sub> cells, CD4 cells)<\/strong> and Cytotoxic T lymphocytes (i.e., Tc cells, Killer T cells, CD8 cells)<\/strong>,\u00a0 through APC display of viral antigens on Class II MHCs and APC release of lymphokines (e.g., monokines and interleukins).<\/li>\n
                    4. Helper and Cytotoxic T lymphocytes with T cell receptors (TCRs)<\/strong> that match\/bind to the viral antigen being presented will proliferate producing daughter TH<\/sub> cells, daughter Memory\u00a0TH <\/sub>cells, daughter TC<\/sub> cells, daughter TC<\/sub>\u00a0 Memory cells, daughter TR<\/sub> Regulatory cells.<\/li>\n
                    5. TH<\/sub> cells are instrumental in activating TC<\/sub> cells and do so by binding viral antigen to TCR and releasing lymphokines.<\/li>\n
                    6. Active TC<\/sub> cells go on a search and destroy (seek and destroy mission) mission to destroy HPV viral antigens. Memory T cells allow for prolonged memory and faster response times during Secondary Response.<\/li>\n
                    7. Activation of B lymphocytes begin with viral antigen binding to their IgD receptors and intake\/phagocytosis of viral proteins \u2013 to become sensitized. Then, B cells display viral proteins on Class II MHCs and bind to Helper T cells that have also been activated (by their TCR binding to viral proteins).<\/li>\n
                    8. Once activated B cells proliferate and their daughter plasma cells produce antibodies against HPV.\u00a0 Their other daughter cells are Memory B cells.<\/li>\n
                    9. Antibodies travel the bloodstream (and other regions) to bind viral antigen, targeting it for destruction.<\/li>\n
                    10. Regulatory T cells will de-activate the B and T cell response once the viral antigen or infection has been eliminated.<\/li>\n
                    11. The build up of Memory B, Memory TH<\/sub> cells, and Memory T<\/span>C<\/sub> cells allows for a very rapid (secondary) response the next time the person is exposed to HPV, meaning that it can eliminate the virus before it has a chance to enter cells and cause cancer.<\/span><\/li>\n<\/ol>\n","protected":false},"author":1370,"menu_order":17,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-4840","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":25,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4840","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":5,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4840\/revisions"}],"predecessor-version":[{"id":4856,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4840\/revisions\/4856"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/25"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/4840\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=4840"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=4840"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=4840"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=4840"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}