Aa
cunnilingus
A simple question: why the cunnilingus is considered sure, and the insertive vaginal intercourse is considered at risk?
It is very frequent having small cuts in mouth (for example, after to have washed the teeth): why the active subject doesn't risk?
It seems more risky that, than a vaginal insertive with a skin-intact penis.
What do you think about it?
It is very frequent having small cuts in mouth (for example, after to have washed the teeth): why the active subject doesn't risk?
It seems more risky that, than a vaginal insertive with a skin-intact penis.
What do you think about it?
Another thought: if "saliva may be protective against HIV-1 infection via the oral route", you would trust to lick a bleeding cut?
Thank you all.
So, in according with Dumbo, "The doctor has said many many times to people concerned about fingering a vagina with cuts on their fingers that it is not a risk....does it not make sense then that an intact penis that goes into a vagina is also very low risk?"
But, looking at the abstract about cervice fluids, I think that inserting a finger, with cuts, deep into vagina is risky.
And further, I'm asking to myself if the cervical fluids don't go out from vagina, or remain inside (that seems very strange!)
Bottom line: it's better to stay at home and masturbating!
So, in according with Dumbo, "The doctor has said many many times to people concerned about fingering a vagina with cuts on their fingers that it is not a risk....does it not make sense then that an intact penis that goes into a vagina is also very low risk?"
But, looking at the abstract about cervice fluids, I think that inserting a finger, with cuts, deep into vagina is risky.
And further, I'm asking to myself if the cervical fluids don't go out from vagina, or remain inside (that seems very strange!)
Bottom line: it's better to stay at home and masturbating!
I only try to de-dramatize.
If I posted my question, it was not for "love of science", or for "joke" but to clarifying a real problem: haw is risky vaginal intercourse.
From all I read from this topic (thanks to Worried_in_MW for his interesting excursus), I think that the problem of vaginal secretion is not definitively clarified by the doctors.
Best wishes to all.
If I posted my question, it was not for "love of science", or for "joke" but to clarifying a real problem: haw is risky vaginal intercourse.
From all I read from this topic (thanks to Worried_in_MW for his interesting excursus), I think that the problem of vaginal secretion is not definitively clarified by the doctors.
Best wishes to all.
Your "joke" was not obvious. This is the net and it it understandably hard to "hear" and see how speech is presented. I took it the same way monkeyflower did.
Anyway, ya, stay home and masturbate, you'll probably feel better for doing so.
Anyway, ya, stay home and masturbate, you'll probably feel better for doing so.
Here is your answer. I cannot take credit for all this research.
Let me know if you have any questions after reading this.
Cunnilingus does not pose a significant risk for HIV for two main reasons.
The first is the multiple HIV inhibiting properties in human saliva:
Human oral epithelial beta-defensins block HIV-1 infection
Last Updated: 2003-11-04 16:31:12 -0400 (Reuters Health)
By Megan Rauscher
NEW YORK (Reuters Health) - Researchers report that HIV-1 induces human beta-defensin (hBD) expression in normal human oral epithelial cells and blocks HIV-1 infectivity.
This may explain why transmission of HIV through oral secretions is uncommon and lead to ways to prevent HIV infection at more susceptible mucosal sites such as the colorectal and vaginal lining, said Dr. Aaron Weinberg from Case Western Reserve University. Dr. Weinberg led a Cleveland, Ohio-based team who reports their discovery in a "Fast Track" paper in the November 7th issue of the journal AIDS.
Natural antimicrobial hBDs are ubiquitous to mucosal linings, including the oral cavity, tracheal lining, the skin, the urogenital lining, and the gastrointestinal lining.
At mucosal sites other than the mouth, hBDs are induced only when the mucosa is injured. "In the mouth, they are induced above baseline levels always and we've discovered that there are certain organisms unique to our oral cavity that have the ability to induce these beta defensins," Dr. Weinberg told Reuters Health.
In their experiments, HIV-1 induced expression of hBD-2 and hBD-3 mRNA 4- to 78-fold, respectively, above baseline in normal oral epithelial cells. "These beta defensins, once induced, have antiretroviral activity," Dr. Weinberg said. "HIV-1 failed to infect these cells, even after 5 days of exposure," he and colleagues note in their report.
hBD-2 and hBD-3 appear to block HIV-1 replication by interacting directly with infectious virions and down-modulating the CXCR4 coreceptor.
"We have a hunch that the oral cavity is uniquely inherently resistant to HIV infectivity," Dr. Weinberg told Reuters Health. "And what we can learn biologically from the oral cavity may help us understand why other sites such as the colorectal and vaginal lining are so susceptible to HIV infection, comparatively speaking."
Ideally, he said, "if we can isolate the organisms from the oral cavity that induce beta-defensins, generate them recombinantly, and apply it to the susceptible sites, we can artificially and locally induce these beta-defensins under normal conditions to prevent prophylactically HIV infectivity." M o r e l i n k s a n d a b s t r a c t s :
STUDY SHOWS COMPONENT OF SALIVA IS VERY EFFECTIVE IN BLOCKING AIDS VIRUS
Potential for Use In Preventing Sexual Transmission of HIV
New York, NY (January 7, 1998) -- Research conducted at The New York Hospital-Cornell University Medical College has found that a natural component of human saliva has a very powerful effect in blocking the growth of laboratory strains of HIV as well as AIDS viruses taken directly from patients. This finding could lead to the development of natural inhibitors to HIV transmission. In a study published in the January 5 issue of the Journal of Experimental Medicine, Dr. Jeffrey Laurence, Director of the Laboratory for AIDS Virus Research; Dr. Ralph Nachman, Chairman of the Department of Medicine; Dr. Roy L. Silverstein, Chief of the Division of Hematology-Oncology; and a team of biomedical scientists describe how they have identified a natural sugar-protein, concentrated in saliva, known as TSP (thrombospondin), and discovered its remarkable ability to block the growth of the AIDS virus. Recognizing that over the past years several labs have found a variety of substances in human saliva that partially inhibit the growth of HIV, Dr. Laurence and his research team delved further into this phenomenon.
Dr. Laurence said, "We began by exploring why there is so little HIV virus in saliva, while large amounts of the virus are found in other body fluids; and why human saliva is so effective at blocking the growth of the AIDS virus in the test tube. This led us to the discovery of TSP." According to Dr. Laurence, "We made the observation that thrombospondin type 1 (TSP-1) can block HIV-1 infection of primary human cells and transform human cell lines of T lymphocyte and monocyte lineages. TSP is effective against both laboratory-adapted strains of HIV-1 and HIV-1 patient isolates. It is active at physiologic concentrations. Saliva experiments indicate that TSP-1 is a major component of the natural HIV inhibitory capacity of saliva." TSP is of particular interest as a natural inhibitor, as others have shown that it may promote wound healing, and suppression of some bacterial infections. Higher levels of TSP in the saliva of some male, as opposed to female, animals may relate to the more frequent wounding of male animals. Wound licking, with application of saliva molecules that could inhibit infection, would then be very beneficial. Speaking of the application of this research, Dr. Nachman said, "This is an exciting finding that is another step forward in our research efforts aimed at preventing AIDS transmission. TSP derivatives could potentially be used vaginally, rectally and orally in condoms, foams, suppositories, mouthwashes and toothpastes to inhibit transmission of the AIDS virus."
While TSP is a very large molecule that would be unwieldy to use directly in patients, the Cornell research team also investigated the mechanism of action of TSP. They found that peptides -- small pieces of the larger TSP -- could block binding of the AIDS virus to its receptor on immune cells. This offers the potential for direct use of these smaller molecules to prevent sexual transmission of HIV. Funding for this work was provided by the Dental, Heart/Lung/Blood, and Allergy/Immunology Institutes of the NIH.
Salivary HIV-1 Inhibitors
P.I.: Murray R. Robinovitch, Professor and Chairman, Department of Oral Biology, School of Dentistry, University of Washington
The specific aims of this study are to identify, isolate and characterize those non-immunoglobulin components of saliva that inhibit HIV-l infectivity and to elucidate their mechanisms of action. We found that adapted the multinuclear activation of a galactosidase indicator assay (MAGI) and the secretory leukocyte protease inhibitor assay (SLPI) for use in the studies. Of seven chromatographically separated components of saliva, those containing non-glycosylated basic proine-rich proteins inhibited HIV-l from 20 to 80% at protein concentrations within physiologic range. The fractions were inhibitory using both assays. The site of action appears to be prior to or at the site of viral entry into the cell rather than later in the infection process.
The modes of transmission of human acquired immunodeficiency syndrome (AIDS) are still not completely understood even though bodily fluids such as blood and semen of infected subjects are regarded as extremely hazardous. Other human secretions such as milk and saliva have been reported to contain inhibitors of HIV-1 infectivity and it is now known that saliva may contain non-immunoglobulin inhibitors as well as secretory immunoglobulins if the subject is infected with HIV. The degree to which a non-infected person_s saliva may be protective against HIV-1 infection via the oral route, and the degree to which the non-immunoglobulin factors and antibodies in an infected subject_s saliva may lessen the biohazard of this secretion is not known. Such information is vital from a public health point of view, and is also extremely important to the practice of dentistry. With such information, better advice can be offered to the public on how to contain AIDS, and to the profession of dentistry on how to design office practices and procedures.
Saliva neutralizes HIV-1 infection by displacing envelope gp120 from the virion.
Int Conf AIDS 1998 Jun 28-Jul 3; 12:267 (abstract no. 21143)
Malamud D, Nagashunmugan T, Friedman HM, Davis CA, Abrams WR
Dept. Biochemistry Univ. Penn Dental Med., Phila 19104-6003, USA.
BACKGROUND: Incubation of HIV-1 with human saliva decreases infectivity. This inhibition is specific for HIV-1, with no effect on adenovirus, HIV-2 or SIV and appears to work at the level of the virus rather than the host cell. We have now identified an active protein fraction and provide evidence that the mechanism of action involves stripping of gp120 from the virus.
METHODS: HIV-1 (laboratory strains and primary isolates) was grown in PBMCs and purified by centrifugation and chromatography on Sephacryl 1000. Submandibular saliva from seronegative donors, or fractions obtained after anion exchange chromatography, were incubated with HIV-1, and then tested for infectivity with HeLa CD4 cells or PBMCs as compared to virus incubated with media only. To test for effects of salivary proteins on gp120-CD4 binding, gp120 binding to immobilized CD4 (NEN-drugquest) was utilized. To detect gp120 stripping, virus treated with media or salivary proteins was analyzed after sucrose gradient centrifugation (10-60% sucrose) or centrifugation at 145,000 x g on a 5% sucrose cushion. Supernatant and pellet were analyzed by ELISA and Western blotting using antibodies to p24 and gp120.
RESULTS: Submandibular saliva did not block the binding of gp120 to immobilized CD4. Incubation of saliva with laboratory strains or primary isolates of HIV-1 resulted in a shift of approximately 50% of the gp120 from the viral pellet to the supernatant. After anion exchange chromatography of submandibular saliva we identified a fraction which inhibited HIV-1 infectivity. This fraction contained two high molecular weight sialyated glycoproteins, and several lower molecular weight proteins. This active fraction also stripped gp120 from the virus.
CONCLUSION: The specific inhibition of HIV-1 infectivity by human submandibular saliva is associated with removal of gp120 from the virus. The active fraction contains several proteins, including two high molecular weight glycoproteins.
Mechanisms of anti-HIV-1 activity of human submandibular saliva.
Conf Retroviruses Opportunistic Infect 1997 Jan 22-26; 4th:140 (abstract no. 412)
Nagashunmugam T, Malamud D, Davis C, Friedman HM; University of Pennsylvania, Philadelphia, PA.
Human submandibular saliva contains factors that reduces HIV-1 infectivity in vitro. The mechanism of action of these salivary proteins is unknown. We asked if salivary proteins act at the level of the virus or, instead, on the host cell. Monoclonal antibodies were used to detect cell surface receptors (CD3, CD4, CD7, HLA-DR, LFA-1, and LFA2) on peripheral blood derived mononuclear cells (PBMCs) treated with media or saliva. Our results show that saliva did not block these receptors nor lower the intensity of detection. PBMCs pretreated with saliva showed no inhibition when subsequently infected with HIV-1HxB2. These results suggest that saliva does not exhibit anti-viral activity by modifying the host cell. Saliva did not block binding of gp120 to CD4 nor did it lyse the virus. Incubation of HIV with submandibular saliva did lead to viral aggregation. Virus-saliva aggregates were subjected to centrifugation on a 10-60% sucrose gradient, fractionated and assayed for p24 antigen. The HIV-saliva complex sediments at a higher density compared with virus alone. Analysis of the gradient fractions for gp120 shows that the env protein is displaced from the virion. These results suggest that one mechanism of salivary anti-HIV activity involves removal of gp120 thereby decreasing HIV infectivity. This work was supported by NIH grants DE09569 and RR00040.
The second is the fact that the vaginal secretions released during cunnilingus are relatively uninfectious. Scientific research regarding women
Let me know if you have any questions after reading this.
Cunnilingus does not pose a significant risk for HIV for two main reasons.
The first is the multiple HIV inhibiting properties in human saliva:
Human oral epithelial beta-defensins block HIV-1 infection
Last Updated: 2003-11-04 16:31:12 -0400 (Reuters Health)
By Megan Rauscher
NEW YORK (Reuters Health) - Researchers report that HIV-1 induces human beta-defensin (hBD) expression in normal human oral epithelial cells and blocks HIV-1 infectivity.
This may explain why transmission of HIV through oral secretions is uncommon and lead to ways to prevent HIV infection at more susceptible mucosal sites such as the colorectal and vaginal lining, said Dr. Aaron Weinberg from Case Western Reserve University. Dr. Weinberg led a Cleveland, Ohio-based team who reports their discovery in a "Fast Track" paper in the November 7th issue of the journal AIDS.
Natural antimicrobial hBDs are ubiquitous to mucosal linings, including the oral cavity, tracheal lining, the skin, the urogenital lining, and the gastrointestinal lining.
At mucosal sites other than the mouth, hBDs are induced only when the mucosa is injured. "In the mouth, they are induced above baseline levels always and we've discovered that there are certain organisms unique to our oral cavity that have the ability to induce these beta defensins," Dr. Weinberg told Reuters Health.
In their experiments, HIV-1 induced expression of hBD-2 and hBD-3 mRNA 4- to 78-fold, respectively, above baseline in normal oral epithelial cells. "These beta defensins, once induced, have antiretroviral activity," Dr. Weinberg said. "HIV-1 failed to infect these cells, even after 5 days of exposure," he and colleagues note in their report.
hBD-2 and hBD-3 appear to block HIV-1 replication by interacting directly with infectious virions and down-modulating the CXCR4 coreceptor.
"We have a hunch that the oral cavity is uniquely inherently resistant to HIV infectivity," Dr. Weinberg told Reuters Health. "And what we can learn biologically from the oral cavity may help us understand why other sites such as the colorectal and vaginal lining are so susceptible to HIV infection, comparatively speaking."
Ideally, he said, "if we can isolate the organisms from the oral cavity that induce beta-defensins, generate them recombinantly, and apply it to the susceptible sites, we can artificially and locally induce these beta-defensins under normal conditions to prevent prophylactically HIV infectivity." M o r e l i n k s a n d a b s t r a c t s :
STUDY SHOWS COMPONENT OF SALIVA IS VERY EFFECTIVE IN BLOCKING AIDS VIRUS
Potential for Use In Preventing Sexual Transmission of HIV
New York, NY (January 7, 1998) -- Research conducted at The New York Hospital-Cornell University Medical College has found that a natural component of human saliva has a very powerful effect in blocking the growth of laboratory strains of HIV as well as AIDS viruses taken directly from patients. This finding could lead to the development of natural inhibitors to HIV transmission. In a study published in the January 5 issue of the Journal of Experimental Medicine, Dr. Jeffrey Laurence, Director of the Laboratory for AIDS Virus Research; Dr. Ralph Nachman, Chairman of the Department of Medicine; Dr. Roy L. Silverstein, Chief of the Division of Hematology-Oncology; and a team of biomedical scientists describe how they have identified a natural sugar-protein, concentrated in saliva, known as TSP (thrombospondin), and discovered its remarkable ability to block the growth of the AIDS virus. Recognizing that over the past years several labs have found a variety of substances in human saliva that partially inhibit the growth of HIV, Dr. Laurence and his research team delved further into this phenomenon.
Dr. Laurence said, "We began by exploring why there is so little HIV virus in saliva, while large amounts of the virus are found in other body fluids; and why human saliva is so effective at blocking the growth of the AIDS virus in the test tube. This led us to the discovery of TSP." According to Dr. Laurence, "We made the observation that thrombospondin type 1 (TSP-1) can block HIV-1 infection of primary human cells and transform human cell lines of T lymphocyte and monocyte lineages. TSP is effective against both laboratory-adapted strains of HIV-1 and HIV-1 patient isolates. It is active at physiologic concentrations. Saliva experiments indicate that TSP-1 is a major component of the natural HIV inhibitory capacity of saliva." TSP is of particular interest as a natural inhibitor, as others have shown that it may promote wound healing, and suppression of some bacterial infections. Higher levels of TSP in the saliva of some male, as opposed to female, animals may relate to the more frequent wounding of male animals. Wound licking, with application of saliva molecules that could inhibit infection, would then be very beneficial. Speaking of the application of this research, Dr. Nachman said, "This is an exciting finding that is another step forward in our research efforts aimed at preventing AIDS transmission. TSP derivatives could potentially be used vaginally, rectally and orally in condoms, foams, suppositories, mouthwashes and toothpastes to inhibit transmission of the AIDS virus."
While TSP is a very large molecule that would be unwieldy to use directly in patients, the Cornell research team also investigated the mechanism of action of TSP. They found that peptides -- small pieces of the larger TSP -- could block binding of the AIDS virus to its receptor on immune cells. This offers the potential for direct use of these smaller molecules to prevent sexual transmission of HIV. Funding for this work was provided by the Dental, Heart/Lung/Blood, and Allergy/Immunology Institutes of the NIH.
Salivary HIV-1 Inhibitors
P.I.: Murray R. Robinovitch, Professor and Chairman, Department of Oral Biology, School of Dentistry, University of Washington
The specific aims of this study are to identify, isolate and characterize those non-immunoglobulin components of saliva that inhibit HIV-l infectivity and to elucidate their mechanisms of action. We found that adapted the multinuclear activation of a galactosidase indicator assay (MAGI) and the secretory leukocyte protease inhibitor assay (SLPI) for use in the studies. Of seven chromatographically separated components of saliva, those containing non-glycosylated basic proine-rich proteins inhibited HIV-l from 20 to 80% at protein concentrations within physiologic range. The fractions were inhibitory using both assays. The site of action appears to be prior to or at the site of viral entry into the cell rather than later in the infection process.
The modes of transmission of human acquired immunodeficiency syndrome (AIDS) are still not completely understood even though bodily fluids such as blood and semen of infected subjects are regarded as extremely hazardous. Other human secretions such as milk and saliva have been reported to contain inhibitors of HIV-1 infectivity and it is now known that saliva may contain non-immunoglobulin inhibitors as well as secretory immunoglobulins if the subject is infected with HIV. The degree to which a non-infected person_s saliva may be protective against HIV-1 infection via the oral route, and the degree to which the non-immunoglobulin factors and antibodies in an infected subject_s saliva may lessen the biohazard of this secretion is not known. Such information is vital from a public health point of view, and is also extremely important to the practice of dentistry. With such information, better advice can be offered to the public on how to contain AIDS, and to the profession of dentistry on how to design office practices and procedures.
Saliva neutralizes HIV-1 infection by displacing envelope gp120 from the virion.
Int Conf AIDS 1998 Jun 28-Jul 3; 12:267 (abstract no. 21143)
Malamud D, Nagashunmugan T, Friedman HM, Davis CA, Abrams WR
Dept. Biochemistry Univ. Penn Dental Med., Phila 19104-6003, USA.
BACKGROUND: Incubation of HIV-1 with human saliva decreases infectivity. This inhibition is specific for HIV-1, with no effect on adenovirus, HIV-2 or SIV and appears to work at the level of the virus rather than the host cell. We have now identified an active protein fraction and provide evidence that the mechanism of action involves stripping of gp120 from the virus.
METHODS: HIV-1 (laboratory strains and primary isolates) was grown in PBMCs and purified by centrifugation and chromatography on Sephacryl 1000. Submandibular saliva from seronegative donors, or fractions obtained after anion exchange chromatography, were incubated with HIV-1, and then tested for infectivity with HeLa CD4 cells or PBMCs as compared to virus incubated with media only. To test for effects of salivary proteins on gp120-CD4 binding, gp120 binding to immobilized CD4 (NEN-drugquest) was utilized. To detect gp120 stripping, virus treated with media or salivary proteins was analyzed after sucrose gradient centrifugation (10-60% sucrose) or centrifugation at 145,000 x g on a 5% sucrose cushion. Supernatant and pellet were analyzed by ELISA and Western blotting using antibodies to p24 and gp120.
RESULTS: Submandibular saliva did not block the binding of gp120 to immobilized CD4. Incubation of saliva with laboratory strains or primary isolates of HIV-1 resulted in a shift of approximately 50% of the gp120 from the viral pellet to the supernatant. After anion exchange chromatography of submandibular saliva we identified a fraction which inhibited HIV-1 infectivity. This fraction contained two high molecular weight sialyated glycoproteins, and several lower molecular weight proteins. This active fraction also stripped gp120 from the virus.
CONCLUSION: The specific inhibition of HIV-1 infectivity by human submandibular saliva is associated with removal of gp120 from the virus. The active fraction contains several proteins, including two high molecular weight glycoproteins.
Mechanisms of anti-HIV-1 activity of human submandibular saliva.
Conf Retroviruses Opportunistic Infect 1997 Jan 22-26; 4th:140 (abstract no. 412)
Nagashunmugam T, Malamud D, Davis C, Friedman HM; University of Pennsylvania, Philadelphia, PA.
Human submandibular saliva contains factors that reduces HIV-1 infectivity in vitro. The mechanism of action of these salivary proteins is unknown. We asked if salivary proteins act at the level of the virus or, instead, on the host cell. Monoclonal antibodies were used to detect cell surface receptors (CD3, CD4, CD7, HLA-DR, LFA-1, and LFA2) on peripheral blood derived mononuclear cells (PBMCs) treated with media or saliva. Our results show that saliva did not block these receptors nor lower the intensity of detection. PBMCs pretreated with saliva showed no inhibition when subsequently infected with HIV-1HxB2. These results suggest that saliva does not exhibit anti-viral activity by modifying the host cell. Saliva did not block binding of gp120 to CD4 nor did it lyse the virus. Incubation of HIV with submandibular saliva did lead to viral aggregation. Virus-saliva aggregates were subjected to centrifugation on a 10-60% sucrose gradient, fractionated and assayed for p24 antigen. The HIV-saliva complex sediments at a higher density compared with virus alone. Analysis of the gradient fractions for gp120 shows that the env protein is displaced from the virion. These results suggest that one mechanism of salivary anti-HIV activity involves removal of gp120 thereby decreasing HIV infectivity. This work was supported by NIH grants DE09569 and RR00040.
The second is the fact that the vaginal secretions released during cunnilingus are relatively uninfectious. Scientific research regarding women
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