VPH, VIRUS DEL PAPILOMA HUMANO Y VACUNAS, ACTUALIZACIÓN !
HPV, HUMAN PAPILLOMA VIRUS AND VACCINES, UPDATE !
PUBLICADO 1998, ACTUALIZADO 2017 - 2025
NOTA: PARA OBTENER TODA LA INFORMACIÓN DEBES LEER LOS ENLACES
EDITORIAL ESPAÑOL
===================
Hola amigos de la red DERMAGIC EXPRESS hoy te voy a poner una actualización del VIRUS DEL PAPILOMA HUMANO, VPH.
===================
Hola amigos de la red DERMAGIC EXPRESS hoy te voy a poner una actualización del VIRUS DEL PAPILOMA HUMANO, VPH.
Hecho que inicie hace mas de 20 años con una publicación que
salio a la red en el año 1999, con el nombre de EL VPH Y SU COMPORTAMIENTO EN NUESTRO MUNDO, donde hable del comportamiento de este virus en 43 países y
estaba lejos la aparición de las
VACUNAS
contra el mismo.
En el año 2017 al 2023 hice una actualización y hoy 2025 te
traigo dos versiones actualizadas del VIRUS DEL VPH, esta que
estas leyendo y el enlace que te dejo mas abajo de este texto
publicado con el nombre de
ACTUALIZACIÓN DEL VIRUS DEL PAPILOMA HUMANO (2025).
1.) HISTORIA DEL VIRUS DEL VPH:
El primero en describir el virus del VPH fue el virologo y
patologo Estadounidense Richard Shope en el año 1933, lo cual hizo en verrugas cutáneas de conejos.
Posteriormente en el año de 1974, el medico y virologo Aleman Harald zur Hausen fue el primero en proponer que el virus del VPH podría estar vinculado o relacionado con cancer cervical en humanos, lo cual fue cierto y le valió para ganar el Premio Nobel de Medicina en el año 2008.
Posteriormente en el año de 1974, el medico y virologo Aleman Harald zur Hausen fue el primero en proponer que el virus del VPH podría estar vinculado o relacionado con cancer cervical en humanos, lo cual fue cierto y le valió para ganar el Premio Nobel de Medicina en el año 2008.
A partir de la década de los 80 y años siguientes, se investigo los distintos tipos de VPH, aislándolos y clasificándolos, siendo los primeros, los VPH1, VPH6, VPH11, VPH16 y VPH18, este ultimo asociado a cancer cervical.
2.) CARACTERÍSTICAS DEL VIRUS:
El virus del PAPILOMA HUMANO, VPH es un virus ADN de doble
cadena, perteneciente a la
familia Papillomaviridae.
Se caracteriza por ser un virus de tamaño pequeño y especifico de los
humanos, el cual provoca multiples infecciones en la piel y mucosas,
incluyendo verrugas y neoplasias intraepiteliales en el cuello uterino
de las mujeres, muchas de las cuales evolucionan a cancer.
3.) IMPORTANCIA:
la Importancia de este virus esta dada por tres hechos:
A.- Es el virus de transmisión sexual más común en el mundo.
B.- Cerca del 80% de las personas sexualmente activas lo contraerán alguna vez.
C.- Algunos Genotipos de VPH, como lo son el VPH16 y el VPH18 y
otros mas, son altamente oncogénicos (cancerígenos), a los cuales se
les atribuye la mayoría de los cánceres cervicouterinos.
4.) CLASIFICACIÓN: (AÑO 2017-2023)
Para el año 2.023 hay aproximadamente 200 tipos de VPH, de los cuales 51 especies afectan la mucosa genital estando
clasificados así:
A.) Mas carcinogénicos los tipos: 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, y
82.
B.) Probable alto riesgo: el 26, 53,y 66.
C.) Bajo riesgo cancerígeno: 6, 11, 40, 42, 43, 44,
54, 61, 70, 72, 73, 81, y 108.
5.) CLASIFICACIÓN ACTUAL (AÑO 2025):
En el año 2012 la Asociación Internacional para la Investigación
del cancer decide modificar esta clasificación, y hoy dia se consideran solo dos (2) tipos: los de
ALTO RIESGO y los
DE BAJO RIESGO, en este enlace encentras la actualización del
VIRUS DEL VPH, PAPILOMA HUMANO, ACTUALIZACIÓN (2025) con mas información y Referencias
bibliográficas.
A.- ALTO RIESGO: El VPH16 y VPH18 siguen siendo los más comunes en cuanto a malignidad representando entre el 70 - 75% de los casos de cáncer cervicouterino a nivel mundial; otros sitios de localización son: ano, vulva, vagina, pene y orofaringe.
B.-Entre el 15 al 20% adicional de casos de malignidad
están representados por los genotipos de
ALTO RIESGO: VPH31, 33,
45, 52 y 58, que en conjunto contribuyen a un 15-20% adicional de los
casos.
C.- Los otros Genotipos que destacan por ser del
ALTO RIESGO, con un 5% de los casos son:
VPH35, 59, 39, 56, 51, 68, 73, 26, 69 y 82, con algunas
variaciones regionales, tal es el caso de áfrica donde prevalece
el VPH35.
D.- En cuanto a los Genotipos de
BAJO RIESGO, los VPH6 y VPH11 son los mas frecuentemente reportados
en la
papilomatosis respiratoria recurrente
y y en las verrugas anogenitales,
NO ASOCIADOS A CANCER.
Se decidió incluir a los subtipos de MODERADO RIESGO
en el grupo de los de
ALTO RIESGO, basados los científicos, en el hecho de que estos finalmente
iban a evolucionar a
MALIGNIDAD.
Todo esto que estas leyendo codujo a los laboratorios a buscar y
crear VACUNAS para proteger a la población mundial de la proliferación
de este VIRUS, adquirido 99,9% por transmisión sexual.
6.) HISTORIA de la creación de las VACUNAS:
A.- En la
década de 1980 comenzó la investigación para la creación de una vacuna,
tras descubrirse la relación existente entre el virus del VPH con
el cáncer cervical.
B.- En 1991,
Ian Fraser y Jian Zhou
(Universidad de Queensland, Australia) lograron desarrollar una
tecnología para crear partículas similares al virus (VLPs),
elemento fundamental para la posible creación de una VACUNA.
Estas partículas (VLPs) fueron creadas mediante ingeniería genética con la finalidad de
estimular el sistema inmune, sin contenido de material genético
viral infeccioso.
C.- En 2006 la primera vacuna fue aprobada en Estados Unidos, por los laboratorios: Merck & Co, (EE.UU.), MSD en Europa y Sanofi-Pasteur, con el nombre comercial de GARDASIL (tetravalente), la cual protege contra los VPH6, VPH11, VPH16, y VPH18 para cáncer cervical, y VPH6 y VPH11 para verrugas genitales.
C.- En 2006 la primera vacuna fue aprobada en Estados Unidos, por los laboratorios: Merck & Co, (EE.UU.), MSD en Europa y Sanofi-Pasteur, con el nombre comercial de GARDASIL (tetravalente), la cual protege contra los VPH6, VPH11, VPH16, y VPH18 para cáncer cervical, y VPH6 y VPH11 para verrugas genitales.
D.- En el año 2007 fua aprobada por la FDA la VACUNA CERVARIX (bivalente) del laboratorio GlaxoSmithKline (GSK, Reino Unido), la cual protege contra los virus VPH16, y VPH18, para evitar fundamentalmente el cáncer cervical, con una cobertura de aproximadamente del 66%, y a la cual también se la atribuye "ALGO" de protección cruzada contra otros tipos de alto riesgo.
E.) En el año 2014-2015
fua aprobada la VACUNA
GARDASIL-9, (nonavalente), una version mas amplia de la
clásica GARDASIL con protección contra los virus:
VPH6, VPH11, VPH16, VPH18, VPH31, VPH33, VPH45, VPH52, VPH58, es decir con
una mayor cobertura (90%), contra los tipos de VPH de
ALTO RIESGO de cáncer
cervical y verrugas.
Los efectos adversos, los cuales suelen ser transitorios y
autolimitados, más frecuentes son:
A.- Locales y leves:
- Dolor.
- Eritema (enrojecimiento) e hinchazón en el sitio de la
inyección.
- Cefalea.
- Mareos.
B .- Moderados a graves:
- Sincope y desmayos: especialmente en adolescentes, por lo que se
recomienda observar al paciente, por lo menos 15 minutos luego
de la administración, con el objetivo de prevenir lesiones
secundarias, en caso de desmayos.
- Pueden ocurrir
reacciones anafilacticas graves
cuando hay alergia comprobada a los componentes de la vacuna, y son
extremadamente raras.
- La incidencia de Sincope y reacciones locales se ha descrito
con mayor frecuencia en la
GARDASIL-9 (nonavalente), en comparación con la clásica GARDASIL (tetravalente).
- Hay ABSOLUTA contraindicacion , cuando se ha comprobado que
el paciente ha experimentado reacciones severas, a la administración
de otras vacunas.
C.- Eventos adversos posteriores
a la vacuna contra el virus del papiloma humano 9-valente
(GARDASIL® 9)
notificados al Sistema de Notificación de Eventos Adversos de Vacunas
(VAERS), 2015-2024:
Eventos no mencionados en la ETIQUETA del producto:
Hubo ademas 57 informes de defunción (MUERTE), de los cuales 18
fueron en mujeres embarazadas, pero los términos o características
neurológicas carecían de patrones etológicos contundentes, de modo que
el sistema VAERS, concluye que dicha vacuna es "segura".
Pero si quieres indagar mas a fondo de lo que ha sucedido con estas
vacunas aquí te dejo el enlace de la publicación
EL SÍNDROME POST VACUNACIÓN GARDASIL Y CERVARIX (2017), el cual "muestra" una cara totalmente a el sistema VAERS del año
2015 al 2024.
8.) CONCLUSIÓN:
Dr. José Lapenta R.
"En un periodo de 23 a 25 años aparecieron unas 120 CEPAS nuevas DEL VIRUS PAPILOMA HUMANO V.P.H, quizá este aumento cabalgante fue lo que llevo a los laboratorios a FABRICAR VACUNAS para esta enfermedad, la experiencia con las mismas ha sido CONTROVERSIAL", pero el hecho de que protejan contra los dos tipos de VPH mas oncogenicos es un "SIGNO POSITIVO."
En este enlace encuentras la publicación ORIGINAL del VIRUS DEL VPH Y SU COMPORTAMIENTO EN EL MUNDO (1999); es importante que te la leas, para que aprendas como ha evolucionado el comportamiento de este virus en la población mundial desde ese año hasta nuestros días.
NOTA: Actualmente estas vacunas tienen un costo de 250$ dolares Americanos en Venezuela.
Saludos a todos!!!Dr. José Lapenta R.
Dr. José M. Lapenta R.,
=================
Hello friends of the DERMAGIC EXPRESS network, today I'm going to give you an UPDATE ON THE HUMAN PAPILLOMAVIRUS (HPV).
This article began more than 20 years ago with a publication published online in 1999, entitled "HPV AND ITS BEHAVIOR IN OUR WORLD." I discussed the behavior of this virus in 43 countries, and the emergence of vaccines against it was still far from complete.
From 2017 to 2023, I updated it, and today, in 2025, I'm bringing you two updated versions of the HPV virus: the one you're reading and the link at the end of this article, published under the name HUMAN PAPILLOMA VIRUS (HPV) UPDATE (2025)."
1.) HISTORY OF THE HPV VIRUS:
The first to describe the HPV virus was the American virologist and pathologist Richard Shope in 1933, which he did in rabbit skin warts.
Later, in 1974, the German physician and virologist Harald zur Hausen was the first to propose that the HPV virus could be linked or related to cervical cancer in humans, which proved true and earned him the Nobel Prize in Medicine in 2008.
Beginning in the 1980s and following years, the different types of HPV were investigated, isolated, and classified. The first were HPV1, HPV6, HPV11, HPV16, and HPV18, the latter being associated with cervical cancer.
2.) CHARACTERISTICS OF THE VIRUS:
The human papillomavirus (HPV) is a double-stranded DNA virus belonging to the Papillomaviridae family.
It is characterized by being a small, human-specific virus that causes multiple skin and mucous membrane infections, including warts and cervical intraepithelial neoplasia in women, many of which progress to cancer.
3.) IMPORTANCE:
The importance of this virus is based on three facts:
A. It is the most common sexually transmitted virus in the world.
B. About 80% of sexually active people will contract it at some point.
C.- Some HPV genotypes, such as HPV16 and HPV18, among others, are highly oncogenic (carcinogenic), and are responsible for the majority of cervical cancers.
4.) CLASSIFICATION: (YEAR 2017-2023):
As of 2023, there are approximately 200 types of HPV, of which 51 species affect the genital mucosa. They are classified as follows:
A.)Most carcinogenic types:
HPV16, HPV18, HPV31, HPV33, HPV35, HPV39, HPV45, HPV51, HPV52,
HPV56, HPV58, HPV59, HPV68, HPV73, and HPV82.
B.) Probable high risk: HPV26, HPV53, and HPV66.
C.) Low carcinogenic risk:
B.) Probable high risk: HPV26, HPV53, and HPV66.
C.) Low carcinogenic risk:
HPV6, HPV11, HPV40, HPV42, HPV43,HPV HPV44,
HPV54, HPV61, HPV70, HPV72, HPV73, HPV81, and HPV108.
5.) CURRENT CLASSIFICATION (YEAR 2025):
In 2012, the International Association for Cancer Research decided to modify this classification, and today only two (2) types are considered: HIGH RISK and LOW RISK. At this link, you will find the update on the HPV, HUMAN PAPILLOMA VIRUS, UPDATE (2025). with more information and bibliographic references.
A.- HIGH RISK: HPV16 and HPV18 continue to be the most common types of malignancy, representing between 70-75% of cervical cancer cases worldwide. Other sites include: anus, vulva, vagina, penis, and oropharynx.
B. Between 15 and 20% of additional malignancy cases are represented by the HIGH-RISK genotypes: HPV31, HPV33, HPV45, HPV52, and HPV58, which together contribute to an additional 15-20% of cases.
C. The other genotypes that stand out as HIGH-RISK, accounting for 5% of cases, are: HPV35, HPV59, HPV39, HPV56, HPV51, HPV68, HPV73, HPV26,
5.) CURRENT CLASSIFICATION (YEAR 2025):
In 2012, the International Association for Cancer Research decided to modify this classification, and today only two (2) types are considered: HIGH RISK and LOW RISK. At this link, you will find the update on the HPV, HUMAN PAPILLOMA VIRUS, UPDATE (2025). with more information and bibliographic references.
A.- HIGH RISK: HPV16 and HPV18 continue to be the most common types of malignancy, representing between 70-75% of cervical cancer cases worldwide. Other sites include: anus, vulva, vagina, penis, and oropharynx.
B. Between 15 and 20% of additional malignancy cases are represented by the HIGH-RISK genotypes: HPV31, HPV33, HPV45, HPV52, and HPV58, which together contribute to an additional 15-20% of cases.
C. The other genotypes that stand out as HIGH-RISK, accounting for 5% of cases, are: HPV35, HPV59, HPV39, HPV56, HPV51, HPV68, HPV73, HPV26,
HPV69, and HPV82, with some regional variations, such as in Africa, where
HPV35 is prevalent.
D.- Regarding the LOW-RISK genotypes, HPV6 and HPV11 are the most frequently reported in recurrent respiratory papillomatosis and anogenital warts, NOT ASSOCIATED WITH CANCER.
It was decided to include the MODERATE RISK subtypes in the HIGH RISK group, based on the scientists' assumption that these would eventually evolve into MALIGNANCY.
All of this you are reading led laboratories to search for and create VACCINES to protect the world's population from the spread of this VIRUS, 99.9% of which is acquired through sexual transmission.
6.) HISTORY OF THE CREATION OF VACCINES:
A.- In the 1980s, research into the creation of a vaccine began after the link between the HPV virus and cervical cancer was discovered.
B.- In 1991, Ian Fraser and Jian Zhou (University of Queensland, Australia) developed a technology to create virus-like particles (VLPs), a fundamental element for the possible creation of a VACCINE.
These particles (VLPs) were created through genetic engineering with the aim of stimulating the immune system, without containing infectious viral genetic material.
C.- In 2006, the first vaccine was approved in the United States by the laboratories: Merck & Co. (USA), MSD in Europe, and Sanofi-Pasteur, under the brand name GARDASIL (tetravalent). It protects against HPV6, HPV11, HPV16, and HPV18 for cervical cancer, and HPV6 and HPV11 for genital warts.
D.- In 2007, the FDA approved the CERVARIX (bivalent) vaccine from GlaxoSmithKline (GSK, United Kingdom). It protects against the HPV16 and HPV18 viruses, primarily to prevent cervical cancer, with a coverage of approximately 66%. It is also attributed with "SOME" cross-protection against other high-risk types.
E.) In 2014-2015, the GARDASIL-9 VACCINE (nine-valent) was approved. This is a broader version of the classic GARDASIL vaccine, offering protection against the following viruses: HPV6, HPV11, HPV16, HPV18, HPV31, HPV33, HPV45, HPV52, and HPV58. This vaccine offers greater coverage (90%) against high-risk HPV types for cervical cancer and warts.
7.) SIDE EFFECTS OF THE VACCINES:
The most common adverse effects, which are usually transient and self-limiting, are:
A.- Local and mild:
- Pain.
- Erythema (redness) and swelling at the injection site.
- Headache.
- Dizziness.
B. Moderate to severe:
- Syncope and fainting: especially in adolescents, so it is recommended that the patient be observed for at least 15 minutes after administration to prevent secondary injuries in the event of fainting.
- Severe anaphylactic reactions can occur when there is a known allergy to vaccine components and are extremely rare.
- The incidence of syncope and local reactions has been reported more frequently with GARDASIL-9 (nine-valent) compared to the classic GARDASIL (four-valent).
- There is an ABSOLUTE contraindication to the administration of other vaccines when the patient has been known to experience severe reactions.
C. Adverse events following the 9-valent human papillomavirus vaccine (GARDASIL® 9) reported to the Vaccine Adverse Event Reporting System (VAERS), 2015-2024:
Events not listed on the product label:
- Postural orthostatic tachycardia syndrome.
- Eye movement disorders.
- Autoimmune thyroiditis.
- Postural abnormality.
There were also 57 reports of deaths, 18 of which were in pregnant women, but the neurological characteristics or features lacked compelling etiological patterns, so the VAERS system concludes that the vaccine is "safe."
But if you want to delve deeper into what has happened with these vaccines, here is the link to the publication "POST-VACCINATION SYNDROME WITH GARDASIL AND CERVARIX" (2017), which completely "shows" the other "face" of the VAERS system from 2015 to 2024.
8.) CONCLUSION:
NOTE: These vaccines currently cost $250 in Venezuela.
D.- Regarding the LOW-RISK genotypes, HPV6 and HPV11 are the most frequently reported in recurrent respiratory papillomatosis and anogenital warts, NOT ASSOCIATED WITH CANCER.
It was decided to include the MODERATE RISK subtypes in the HIGH RISK group, based on the scientists' assumption that these would eventually evolve into MALIGNANCY.
All of this you are reading led laboratories to search for and create VACCINES to protect the world's population from the spread of this VIRUS, 99.9% of which is acquired through sexual transmission.
6.) HISTORY OF THE CREATION OF VACCINES:
A.- In the 1980s, research into the creation of a vaccine began after the link between the HPV virus and cervical cancer was discovered.
B.- In 1991, Ian Fraser and Jian Zhou (University of Queensland, Australia) developed a technology to create virus-like particles (VLPs), a fundamental element for the possible creation of a VACCINE.
These particles (VLPs) were created through genetic engineering with the aim of stimulating the immune system, without containing infectious viral genetic material.
C.- In 2006, the first vaccine was approved in the United States by the laboratories: Merck & Co. (USA), MSD in Europe, and Sanofi-Pasteur, under the brand name GARDASIL (tetravalent). It protects against HPV6, HPV11, HPV16, and HPV18 for cervical cancer, and HPV6 and HPV11 for genital warts.
D.- In 2007, the FDA approved the CERVARIX (bivalent) vaccine from GlaxoSmithKline (GSK, United Kingdom). It protects against the HPV16 and HPV18 viruses, primarily to prevent cervical cancer, with a coverage of approximately 66%. It is also attributed with "SOME" cross-protection against other high-risk types.
E.) In 2014-2015, the GARDASIL-9 VACCINE (nine-valent) was approved. This is a broader version of the classic GARDASIL vaccine, offering protection against the following viruses: HPV6, HPV11, HPV16, HPV18, HPV31, HPV33, HPV45, HPV52, and HPV58. This vaccine offers greater coverage (90%) against high-risk HPV types for cervical cancer and warts.
7.) SIDE EFFECTS OF THE VACCINES:
The most common adverse effects, which are usually transient and self-limiting, are:
A.- Local and mild:
- Pain.
- Erythema (redness) and swelling at the injection site.
- Headache.
- Dizziness.
B. Moderate to severe:
- Syncope and fainting: especially in adolescents, so it is recommended that the patient be observed for at least 15 minutes after administration to prevent secondary injuries in the event of fainting.
- Severe anaphylactic reactions can occur when there is a known allergy to vaccine components and are extremely rare.
- The incidence of syncope and local reactions has been reported more frequently with GARDASIL-9 (nine-valent) compared to the classic GARDASIL (four-valent).
- There is an ABSOLUTE contraindication to the administration of other vaccines when the patient has been known to experience severe reactions.
C. Adverse events following the 9-valent human papillomavirus vaccine (GARDASIL® 9) reported to the Vaccine Adverse Event Reporting System (VAERS), 2015-2024:
Events not listed on the product label:
- Postural orthostatic tachycardia syndrome.
- Eye movement disorders.
- Autoimmune thyroiditis.
- Postural abnormality.
There were also 57 reports of deaths, 18 of which were in pregnant women, but the neurological characteristics or features lacked compelling etiological patterns, so the VAERS system concludes that the vaccine is "safe."
But if you want to delve deeper into what has happened with these vaccines, here is the link to the publication "POST-VACCINATION SYNDROME WITH GARDASIL AND CERVARIX" (2017), which completely "shows" the other "face" of the VAERS system from 2015 to 2024.
8.) CONCLUSION:
"Over a period of 23 to 25 years, some 120 new STRAINS OF THE HUMAN PAPILLOMAVIRUS (HPV) appeared. Perhaps this dramatic increase was what led laboratories to manufacture vaccines for this disease. Experience with these vaccines has been CONTROVERSIAL," but the fact that they protect against the two most oncogenic HPV types is a "POSITIVE SIGN."At this link, you'll find the original publication "HPV VIRUS AND ITS BEHAVIOR IN THE WORLD" (1999). It's important to read it to learn how the behavior of this virus has evolved in the global population from that year to the present.
NOTE: These vaccines currently cost $250 in Venezuela.
Greetings to all!!!
Dr. José Lapenta R.
Dr. José M. Lapenta R.,
=======================================================================
REFERENCIAS BIBLIOGRÁFICAS/ BIBLIOGRAPHICAL REFERENCES
=======================================================================
A.- Adverse events following 9-valent human papillomavirus vaccine (GARDASIL 9) reported to the Vaccine Adverse Event Reporting System (VAERS), 2015-2024.
REFERENCIAS BIBLIOGRÁFICAS/ BIBLIOGRAPHICAL REFERENCES
=======================================================================
A.- Adverse events following 9-valent human papillomavirus vaccine (GARDASIL 9) reported to the Vaccine Adverse Event Reporting System (VAERS), 2015-2024.
=======================================================================
1.) Detection and typing of human papillomaviruses by polymerase chain
reaction in cervical scrapes of Croatian women with abnormal cytology.
(CROATIA)
2.) Risk factors for HPV DNA detection in middle-aged women. (FRANCE)
3.) Human papillomavirus 16 and 18 infection of the uterine cervix in women with different grades of cervical intraepithelial neoplasia (CIN). (SLOVENIA)
4.) HPV 16 infection and progression of cervical intra-epithelial
neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants. (AMSTERDAM)
5.) HPV prevalence among Mexican women with neoplastic and normal cervixes. (MEXICO)
6.) Cigarette smoking and high-risk HPV DNA as predisposing factors for high-grade cervical intraepithelial neoplasia (CIN) in young Brazilian women. (BRAZIL)
7.) Prevalence of human papillomavirus infection in premalignant and malignant lesions of the oral cavity in U.K. subjects: a novel method of detection. (LONDON)
8.) Causes of cervical cancer in the Philippines: a case-control study. (PHILLIPINES)
9.) Novel HPV types present in oral papillomatous lesions from patients with HIV infection. (GERMANY)
10.) HPV-types, cytological and histopathological findings in three groups of women with possible HPV-related disease. (SWEDEN)
11.) A general primer GP5+/GP6(+)-mediated PCR-enzyme immunoassay method for rapid detection of 14 high-risk and 6 low-risk human papillomavirus genotypes in cervical scrapings. (AMSTERDAM)
12.) Prevalence of antibodies to human papillomavirus (HPV) type 16 virus-like particles in relation to cervical HPV infection among college women. (USA)
13.) Detection of human papillomavirus mRNA and cervical cancer cells in peripheral blood of cervical cancer patients with metastasis. (TAIWAN)
14.) Human papillomavirus in tissue of bladder and bladder carcinoma specimens. A preliminary study. (GERMANY)
15.) Detection of human papillomavirus (HPV) type 47 DNA in malignant lesions from epidermodysplasia verruciformis by protocols for precise typing of related HPV DNAs. (JAPAN)
16.) HLA and susceptibility to cervical neoplasia. (NETHERLANDS)
17.) Non-isotopic in situ hybridization of HPV types in cervical intraepithelial lesions in patients with AIDS. (BRAZIL)
18.) HLA-A2-restricted peripheral blood cytolytic T lymphocyte response to HPV type 16 proteins E6 and E7 from patients with neoplastic cervical lesions. (GERMANY)
19.) Human papilloma virus 16-18 infection and cervical cancer in Mexico: a case-control study. (MEXICO)
20.) Detection of human papillomavirus (HPV) type 6, 16 and 18 in head and neck squamous cell carcinomas by in situ hybridization. (CROATIA)
21.) Prevalence of human papillomavirus infection in women attending a sexually transmitted disease clinic. (JAPAN)
22.) Demonstration of multiple HPV types in laryngeal premalignant lesions using polymerase chain reaction and immunohistochemistry. (ITALY)
23.) Adenocarcinoma of the uterine cervix in Ireland and Sweden: human papillomavirus infection and biologic alterations. (IRELAND AND SWEDEN)
24.) Risk factors for high-risk type human papillomavirus infection among Mexican-American women. (USA-MEXICO)
25.) Many different papillomaviruses have low transcriptional activity in spite of strong epithelial specific enhancers. (SINGAPORE)
26.) Low frequency of human papillomavirus infection in initial papillary bladder tumors. (CANADA)
27.) Human papillomavirus genotype spectrum in Czech women: correlation of HPV DNA presence with antibodies against HPV-16, 18, and 33 virus-like particles. (CZECH REPUBLIC)
28.) Mucosal oncogenic human papillomaviruses and extragenital Bowen disease. (FRANCE) 29.) High prevalence of a variety of epidermodysplasia verruciformis-associated human papillomaviruses in psoriatic skin of patients treated or not treated with PUVA. (GERMANY)
30.) Human papillomavirus type 31 oncoproteins E6 and E7 are required for the maintenance of episomes during the viral life cycle in normal human keratinocytes. (USA)
31.) Clinical, histopathologic, and molecular aspects of cutaneous human papillomavirus infections. (USA)
32.) Screening for genital human papillomavirus: results from an international validation study on human papillomavirus sampling techniques. (SPAIN)
33.) Use of the same archival papanicolanou smears for detection of human papillomavirus by cytology and polymerase chain reaction. (AUSTRALIA)
34.) Detection and typing of human papillomavirus in cervical cancer in the Thai. (THAILAND)
35.) Correlation between polymerase chain reaction and cervical cytology for detection of human papillomavirus infection in women with and without dysplasia. (NORWAY)
36.) Detection and quantitation of human papillomavirus by using the fluorescent 5' exonuclease assay. (SWEDEN)
37.) Risk factors for HPV detection in archival Pap smears. A population-based study from Greenland and Denmark. (GREENLAND AND DENMARK)
38.) [Human papillomavirus infection in women with and without abnormal cervical cytology]. (MEXICO)
39.) Follow-up of human papillomavirus (HPV) DNA and local anti-HPVantibodies in cytologically normal pregnant women. (HUNGARY)
40.) Relatively low prevalence of human papillomavirus 16, 18 and 33 DNA inthe normal cervices of Japanese women shown by polymerase chain reaction. (JAPAN)
41.) Comparison of a one-step and a two-step polymerase chain reaction with degenerate general primers in a population-based study of human papillomavirus infection in young Swedish women. (SWEDEN)
42.) Human papillomavirus DNA in unselected pregnant and non-pregnant women. (FINLAND)
43.) Prevalence of HPV cervical infection in a family planning clinic determined by polymerase chain reaction and dot blot hybridisation. (LONDON)
44.) Type-specific prevalence of human papillomavirus DNA among Jamaican colposcopy patients. (JAMAICA)
45.) Polymerase chain reaction detection and restriction enzyme typing of human papillomavirus in cervical carcinoma. (MALAYSIA)
46.) Human papillomavirus (HPV) cervical lesions: results from 300 Italian women studied with DNA hybridization techniques and morphology. (ITALY)
47.) Detection of human papillomavirus (HPV) DNA in human prostatic tissues by polymerase chain reaction (PCR). (USA)
48.) High-risk human papillomavirus types in cytologically normal cervical scrapes from Kenya. (KENYA)
49.) Detection of type specific human papillomavirus (HPV) DNA in cervical cancers of Indian women. (INDIA)
50.) Natural history of cervical human papillomavirus lesions. (JAPAN)
51.) Detection of human papillomavirus types in cervical lesions of patients from Taiwan by the polymerase chain reaction. (TAIWAN)
52.) Human papillomaviruses in cervical cancer I. HPV-16 and 18 predominate in the Greek population. (TAIWAN-CHINA) 53.) The prevalence of cervical infection with human papillomaviruses and cervical dysplasia in Alaska Native women. (ALASKA)
54.) Detection of human papillomaviruses in exfoliated cervicovaginal cells by in situ DNA hybridization analysis. (TAIWAN)
55.) Detection and typing of human papillomavirus in cervical specimens of Turkish women. (TURKEY)
56.) Prevalence of human papillomavirus DNA in cervical tissue. Retrospective analysis of 855 cervical biopsies. (GERMANY)
57.) Prevalence of human papillomavirus DNA in female cervical lesions from Rio de Janeiro, Brazil. (BRAZIL)
58.) Prevalence of human papilloma virus 16 or 18 in cervical cancer in Hualien, eastern Taiwan. (TAIWAN)
59.) Human papillomavirus types 52 and 58 are prevalent in cervical cancers from Chinese women. (CHINA)
60.) Human papillomavirus infection and risk determinants for squamous intraepithelial lesion and cervical cancer in Japan. (JAPAN)
61.) Detection and typing of human papillomavirus in cervical carcinomas in Russian women: a prognostic study. (RUSSIA)
62.) Serologic response to human papillomavirus type 16 (HPV-16) virus-like particles in HPV-16 DNA-positive invasive cervical cancer and cervical intraepithelial neoplasia grade III patients and controls from Colombia and Spain. (COLOMBIA, SPAIN)
63.) Detection of human papillomavirus-related oral verruca vulgaris among Venezuelans. (VENEZUELA)
64.) Oncogenic association of specific human papillomavirus types with cervical neoplasia. (USA, PERU and BRAZIL)
65.) Chromosome fragility in lymphocytes of women with cervical uterine lesions produced by human papillomavirus. (ECUADOR)
66.) Multifocal papilloma virus epithelial hyperplasia [see comments] (GUATEMALA)
67.) Genital human papillomavirus infection in Panama City prostitutes. (PANAMA)
68.) Risk factors for genital papillomavirus infection in populations at high and low risk for cervical cancer. (PANAMA)
69.) Demonstration of multiple HPV types in normal cervix and in cervical squamous cell carcinoma using the polymerase chain reaction on paraffin wax embedded material. (ENGLAND)
70.) Morphological correlation of human papillomavirus infection of matched cervical smears and biopsies from patients with persistent mild cervical cytological abnormalities. (ENGLAND)
71.) Epidermodysplasia verruciformis in Africans. (SOUTH AFRICA)
72.) Transmissibility and treatment failures of different types of human papillomavirus. (ISRAEL)
73.) High frequency of detection of epidermodysplasia verruciformis-associated human papillomavirus DNA in biopsies from malignant and premalignant skin lesions from renal transplant recipients. (THE NETHERLANDS)
===================================================================
2.) Risk factors for HPV DNA detection in middle-aged women. (FRANCE)
3.) Human papillomavirus 16 and 18 infection of the uterine cervix in women with different grades of cervical intraepithelial neoplasia (CIN). (SLOVENIA)
4.) HPV 16 infection and progression of cervical intra-epithelial
neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequence variants. (AMSTERDAM)
5.) HPV prevalence among Mexican women with neoplastic and normal cervixes. (MEXICO)
6.) Cigarette smoking and high-risk HPV DNA as predisposing factors for high-grade cervical intraepithelial neoplasia (CIN) in young Brazilian women. (BRAZIL)
7.) Prevalence of human papillomavirus infection in premalignant and malignant lesions of the oral cavity in U.K. subjects: a novel method of detection. (LONDON)
8.) Causes of cervical cancer in the Philippines: a case-control study. (PHILLIPINES)
9.) Novel HPV types present in oral papillomatous lesions from patients with HIV infection. (GERMANY)
10.) HPV-types, cytological and histopathological findings in three groups of women with possible HPV-related disease. (SWEDEN)
11.) A general primer GP5+/GP6(+)-mediated PCR-enzyme immunoassay method for rapid detection of 14 high-risk and 6 low-risk human papillomavirus genotypes in cervical scrapings. (AMSTERDAM)
12.) Prevalence of antibodies to human papillomavirus (HPV) type 16 virus-like particles in relation to cervical HPV infection among college women. (USA)
13.) Detection of human papillomavirus mRNA and cervical cancer cells in peripheral blood of cervical cancer patients with metastasis. (TAIWAN)
14.) Human papillomavirus in tissue of bladder and bladder carcinoma specimens. A preliminary study. (GERMANY)
15.) Detection of human papillomavirus (HPV) type 47 DNA in malignant lesions from epidermodysplasia verruciformis by protocols for precise typing of related HPV DNAs. (JAPAN)
16.) HLA and susceptibility to cervical neoplasia. (NETHERLANDS)
17.) Non-isotopic in situ hybridization of HPV types in cervical intraepithelial lesions in patients with AIDS. (BRAZIL)
18.) HLA-A2-restricted peripheral blood cytolytic T lymphocyte response to HPV type 16 proteins E6 and E7 from patients with neoplastic cervical lesions. (GERMANY)
19.) Human papilloma virus 16-18 infection and cervical cancer in Mexico: a case-control study. (MEXICO)
20.) Detection of human papillomavirus (HPV) type 6, 16 and 18 in head and neck squamous cell carcinomas by in situ hybridization. (CROATIA)
21.) Prevalence of human papillomavirus infection in women attending a sexually transmitted disease clinic. (JAPAN)
22.) Demonstration of multiple HPV types in laryngeal premalignant lesions using polymerase chain reaction and immunohistochemistry. (ITALY)
23.) Adenocarcinoma of the uterine cervix in Ireland and Sweden: human papillomavirus infection and biologic alterations. (IRELAND AND SWEDEN)
24.) Risk factors for high-risk type human papillomavirus infection among Mexican-American women. (USA-MEXICO)
25.) Many different papillomaviruses have low transcriptional activity in spite of strong epithelial specific enhancers. (SINGAPORE)
26.) Low frequency of human papillomavirus infection in initial papillary bladder tumors. (CANADA)
27.) Human papillomavirus genotype spectrum in Czech women: correlation of HPV DNA presence with antibodies against HPV-16, 18, and 33 virus-like particles. (CZECH REPUBLIC)
28.) Mucosal oncogenic human papillomaviruses and extragenital Bowen disease. (FRANCE) 29.) High prevalence of a variety of epidermodysplasia verruciformis-associated human papillomaviruses in psoriatic skin of patients treated or not treated with PUVA. (GERMANY)
30.) Human papillomavirus type 31 oncoproteins E6 and E7 are required for the maintenance of episomes during the viral life cycle in normal human keratinocytes. (USA)
31.) Clinical, histopathologic, and molecular aspects of cutaneous human papillomavirus infections. (USA)
32.) Screening for genital human papillomavirus: results from an international validation study on human papillomavirus sampling techniques. (SPAIN)
33.) Use of the same archival papanicolanou smears for detection of human papillomavirus by cytology and polymerase chain reaction. (AUSTRALIA)
34.) Detection and typing of human papillomavirus in cervical cancer in the Thai. (THAILAND)
35.) Correlation between polymerase chain reaction and cervical cytology for detection of human papillomavirus infection in women with and without dysplasia. (NORWAY)
36.) Detection and quantitation of human papillomavirus by using the fluorescent 5' exonuclease assay. (SWEDEN)
37.) Risk factors for HPV detection in archival Pap smears. A population-based study from Greenland and Denmark. (GREENLAND AND DENMARK)
38.) [Human papillomavirus infection in women with and without abnormal cervical cytology]. (MEXICO)
39.) Follow-up of human papillomavirus (HPV) DNA and local anti-HPVantibodies in cytologically normal pregnant women. (HUNGARY)
40.) Relatively low prevalence of human papillomavirus 16, 18 and 33 DNA inthe normal cervices of Japanese women shown by polymerase chain reaction. (JAPAN)
41.) Comparison of a one-step and a two-step polymerase chain reaction with degenerate general primers in a population-based study of human papillomavirus infection in young Swedish women. (SWEDEN)
42.) Human papillomavirus DNA in unselected pregnant and non-pregnant women. (FINLAND)
43.) Prevalence of HPV cervical infection in a family planning clinic determined by polymerase chain reaction and dot blot hybridisation. (LONDON)
44.) Type-specific prevalence of human papillomavirus DNA among Jamaican colposcopy patients. (JAMAICA)
45.) Polymerase chain reaction detection and restriction enzyme typing of human papillomavirus in cervical carcinoma. (MALAYSIA)
46.) Human papillomavirus (HPV) cervical lesions: results from 300 Italian women studied with DNA hybridization techniques and morphology. (ITALY)
47.) Detection of human papillomavirus (HPV) DNA in human prostatic tissues by polymerase chain reaction (PCR). (USA)
48.) High-risk human papillomavirus types in cytologically normal cervical scrapes from Kenya. (KENYA)
49.) Detection of type specific human papillomavirus (HPV) DNA in cervical cancers of Indian women. (INDIA)
50.) Natural history of cervical human papillomavirus lesions. (JAPAN)
51.) Detection of human papillomavirus types in cervical lesions of patients from Taiwan by the polymerase chain reaction. (TAIWAN)
52.) Human papillomaviruses in cervical cancer I. HPV-16 and 18 predominate in the Greek population. (TAIWAN-CHINA) 53.) The prevalence of cervical infection with human papillomaviruses and cervical dysplasia in Alaska Native women. (ALASKA)
54.) Detection of human papillomaviruses in exfoliated cervicovaginal cells by in situ DNA hybridization analysis. (TAIWAN)
55.) Detection and typing of human papillomavirus in cervical specimens of Turkish women. (TURKEY)
56.) Prevalence of human papillomavirus DNA in cervical tissue. Retrospective analysis of 855 cervical biopsies. (GERMANY)
57.) Prevalence of human papillomavirus DNA in female cervical lesions from Rio de Janeiro, Brazil. (BRAZIL)
58.) Prevalence of human papilloma virus 16 or 18 in cervical cancer in Hualien, eastern Taiwan. (TAIWAN)
59.) Human papillomavirus types 52 and 58 are prevalent in cervical cancers from Chinese women. (CHINA)
60.) Human papillomavirus infection and risk determinants for squamous intraepithelial lesion and cervical cancer in Japan. (JAPAN)
61.) Detection and typing of human papillomavirus in cervical carcinomas in Russian women: a prognostic study. (RUSSIA)
62.) Serologic response to human papillomavirus type 16 (HPV-16) virus-like particles in HPV-16 DNA-positive invasive cervical cancer and cervical intraepithelial neoplasia grade III patients and controls from Colombia and Spain. (COLOMBIA, SPAIN)
63.) Detection of human papillomavirus-related oral verruca vulgaris among Venezuelans. (VENEZUELA)
64.) Oncogenic association of specific human papillomavirus types with cervical neoplasia. (USA, PERU and BRAZIL)
65.) Chromosome fragility in lymphocytes of women with cervical uterine lesions produced by human papillomavirus. (ECUADOR)
66.) Multifocal papilloma virus epithelial hyperplasia [see comments] (GUATEMALA)
67.) Genital human papillomavirus infection in Panama City prostitutes. (PANAMA)
68.) Risk factors for genital papillomavirus infection in populations at high and low risk for cervical cancer. (PANAMA)
69.) Demonstration of multiple HPV types in normal cervix and in cervical squamous cell carcinoma using the polymerase chain reaction on paraffin wax embedded material. (ENGLAND)
70.) Morphological correlation of human papillomavirus infection of matched cervical smears and biopsies from patients with persistent mild cervical cytological abnormalities. (ENGLAND)
71.) Epidermodysplasia verruciformis in Africans. (SOUTH AFRICA)
72.) Transmissibility and treatment failures of different types of human papillomavirus. (ISRAEL)
73.) High frequency of detection of epidermodysplasia verruciformis-associated human papillomavirus DNA in biopsies from malignant and premalignant skin lesions from renal transplant recipients. (THE NETHERLANDS)
===================================================================
