Antiviral therapy associated with fewer recurring eye problems from herpes simplex virus

ScienceDaily (Sep. 14, 2010) — Taking oral antiviral medications following infection with the herpes simplex virus may be associated with a reduced risk of recurring eye-related manifestations of the disease, according to a report in the September issue of Archives of Ophthalmology, one of the JAMA/Archives journals.

"Herpes simplex virus (HSV) is a common cause of corneal disease and is the leading infectious cause of corneal blindness among developed nations," the authors write as background information in the article. After the initial exposure to the virus and the resulting systemic infection, herpes simplex establishes a latent infection in sensory nerve structures. Reactivation of this latent infection could lead to initial or recurrent disease in one or both eyes, including inflammation or infection of the cornea, eyelid, membrane inside the eye (conjunctivitis, or pink eye) or middle layer of the eye (uveitis).

Ryan C. Young, B.A., of Mayo Clinic, Rochester, Minn., and colleagues estimated the incidence of HSV eye disease in a community-based cohort, in Olmstead County, Minnesota, from 1976 through 2007. During this time period, 394 patients with ocular HSV were identified, for an annual incidence of 11.8 per 100,000 individuals.

Oral antiviral therapy was prescribed in 175 (44 percent) of these patients, who underwent therapy for an average of 2.8 years (36 percent of the average 7.7 years of follow-up). Patients not taking this prophylactic therapy were 9.4 times more likely to have a recurrence of epithelial keratitis (infection of the top layer of the cornea), 8.4 times more likely to have a recurrence of stromal keratitis (infection of deeper layers of the cornea) and 34.5 times more likely to have a recurrence of blepharitis (eyelid infection) or conjunctivitis than those taking antiviral medications.

A total of 20 patients experienced adverse outcomes, including visual loss and perforation of the cornea; of these, 17 (85 percent) were not taking oral antiviral prophylaxis.

"Overall, this community-based retrospective study demonstrated a stable incidence of HSV eye disease during a recent 32-year period," the authors write. "We found a more dramatic protective effect of oral antiviral prophylaxis on recurrences of ocular HSV than had been described previously."

"The results of this study suggest that oral antiviral prophylaxis should be considered for patients with frequent recurrences of corneal disease," they conclude. "Additionally, we recommend an evaluation of the possible barriers preventing compliance with antiviral prophylaxis and a reassessment of the cost-effectiveness of long-term oral antiviral therapy."

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The above story is reprinted from materials provided by JAMA and Archives Journals.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Ryan C. Young; David O. Hodge; Thomas J. Liesegang; Keith H. Baratz. Incidence, Recurrence, and Outcomes of Herpes Simplex Virus Eye Disease in Olmsted County, Minnesota, 1976-2007: The Effect of Oral Antiviral Prophylaxis. Arch Ophthalmol, 2010; 128 (9): 1178-1183 [link]

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Map of herpes virus protein suggests a new drug therapy

ScienceDaily (July 8, 2010) — The mechanism by which a herpes virus invades cells has remained a mystery to scientists seeking to thwart this family of viruses. New research funded by the National Institutes of Health and published online in advance of print in Nature Structural & Molecular Biology reveals the unusual structure of the protein complex that allows a herpes virus to invade cells. This detailed map of a key piece of the herpes virus "cell-entry machinery" gives scientists a new target for antiviral drugs.

"Most viruses need cell-entry proteins called fusogens in order to invade cells. We have known that the herpes virus fusogen does not act alone and that a complex of two other viral cell-entry proteins is always required. We expected that this complex was also a fusogen, but after determining the structure of this key protein complex, we found that it does not resemble other known fusogens," said senior author Ekaterina Heldwein, PhD, assistant professor in the molecular biology and microbiology department at Tufts University School of Medicine.

"This unexpected result leads us to believe that this protein complex is not a fusogen itself but that it regulates the fusogen. We also found that certain antibodies interfere with the ability of this protein complex to bind to the fusogen, evidence that antiviral drugs that target this interaction could prevent viral infection," Heldwein continued. Heldwein is also a member of the biochemistry and molecular microbiology program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts.

"Katya Heldwein's work has resulted in a map of the protein complex needed to trigger herpes virus infection. The NIH Director's New Innovator Awards are designed to support such breakthroughs. This research not only adds to what we know about how herpes viruses infect mammalian cells, but also sets the stage for new therapeutics that restrict herpes virus's access to the cell," said Jeremy M. Berg, PhD, director of the National Institute of General Medical Sciences (NIGMS) at the National Institutes of Health.

"We hope that determining the structure of this essential piece of the herpes virus cell-entry machinery will help us answer some of the many questions about how herpes virus initiates infection. Knowing the structures of cell-entry proteins will help us find the best strategy for interfering with this pervasive family of viruses," said first author Tirumala K. Chowdary, PhD, a postdoctoral associate in the department of molecular biology and microbiology at TUSM and member of Heldwein's lab.

Currently, there is no cure for herpes viruses. Upon infection, the viruses remain in the body for life and can stay inactive for long periods of time. When active, however, different herpes viruses can cause cold sores, blindness, encephalitis, or cancers. More than half of Americans are infected with herpes simplex virus type 1 (HSV-1), which causes cold sores, by the time they reach their 20s. Currently, about one in six Americans is infected with herpes simplex virus type 2 (HSV-2), the virus responsible for genital herpes. Complications of HSV-2, a sexually-transmitted disease, include recurrent painful genital sores, psychological distress, and, if transmitted from mother to child, potentially fatal infections in newborn infants.

Heldwein teamed up with colleagues at University of Pennsylvania and used x-ray crystallography along with cell microscopy techniques to study the structure and function of this cell-entry protein complex in HSV-2. Heldwein is currently developing a molecular movie that illustrates how herpes virus enters the cell.

Additional authors are Tina Cairns, PhD, a research specialist; Doina Atanasiu, a research associate; and Gary Cohen, PhD, professor and chair, all in the department of microbiology at the University of Pennsylvania School of Dental Medicine; and Roselyn Eisenberg, PhD, professor in the department of microbiology at the University of Pennsylvania School of Veterinary Medicine.

This work was funded by the Office of the Director of the National Institutes of Health, through a New Innovator Award in 2007 to Ekaterina Heldwein. The New Innovator Awards, part of the NIH Roadmap for Medical Research initiative, are awarded to support early-career scientists who take innovative -- and potentially transformative -- approaches to major challenges in biomedical research. The work was also funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, and the Pew Scholar Program in Biomedical Sciences.

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The above story is reprinted from materials provided by Tufts University, Health Sciences.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Tirumala K Chowdary, Tina M Cairns, Doina Atanasiu, Gary H Cohen, Roselyn J Eisenberg, Ekaterina E Heldwein. Crystal structure of the conserved herpesvirus fusion regulator complex gH-gL. Nature Structural & Molecular Biology, 2010; DOI: 10.1038/nsmb.1837

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Immunogene therapy combined with standard treatment is safe for patients with brain tumors, study suggests

ScienceDaily (Sep. 6, 2011) — A clinical trial has shown that a form of gene therapy is safe for treating a deadly form of brain cancer, even when combined with radiation therapy.

The phase 1b trial was conducted at the Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James) and at Methodist at Hospital in Houston, TX.

The novel treatment uses an adenovirus vector called AdV-tk. The vector is taken up by cancer cells where it activates a drug that kills the cells. The vector is applied in the operating room after removing brain tumors such as glioblastoma multiforme, the most common and dangerous form of brain cancer.

The findings, published online in the Journal of Clinical Oncology, suggest that the therapy might also stimulate an immune response against the tumor.

"This is the first time that a gene therapy approach was combined with radiation in patients with newly diagnosed glioblastoma," says first author Dr. E. Antonio Chiocca, professor and chair of neurological surgery and co-director of the Dardinger Center for Neuro-oncology and Neurosciences at Ohio State.

"There had been a concern that combining these two treatments could be too toxic for patients, but this was not the case. We do not know yet if this will improve survival, but these findings are encouraging," he says.

Glioblastomas occur in about 18,500 Americans annually and kill nearly 13,000 of them yearly. Glioblastoma multiforme is the most common and lethal form of the malignancy, with an average survival of 15 months after diagnosis.

The tumors often recur because cancer cells typically migrate into adjacent brain tissue where they can give rise to a recurrent tumor. This study examines an immunogene therapy approach that is designed to kill these undetected cancer cells and prevent recurrence.

This clinical trial involved 10 patients with glioblastoma multiforme and two patients with anaplastic astrocytoma. The procedure works as follows:

After removing the tumor, the neurosurgeon injects the tumor bed with 1 milliliter (1/30th oz) of a solution containing the AdV-tk vector. The vector carries a gene from herpes simplex virus for an enzyme called thymidine kinase (the '-tk' in AdV-tk). Cancer cells infected with the vector begin making the enzyme.Patients then take the anti-herpes virus drug valacyclovir for two weeks.Inside the cancer cells, the herpes thymidine kinase enzyme converts valacyclovir into DNA building blocks that the rapidly growing cancer cells cannot use to make DNA, and this kills them.Radiation therapy begins halfway through the course of valacyclovir. The radiation damages the DNA in the cancer cells, which then try to repair it, using the toxic valacyclovir building blocks.

In addition to improved overall survival, studies revealed a significant rise in the number of T lymphocytes in the tumors. This suggests that the gene therapy stimulated an immune response against the tumor, producing an "immunogene therapy" effect.

Cancer immunogene therapy refers to genetically manipulating cancer cells to stimulate an immune response against a tumor. (Note: This differs from "immunotherapy," which attempts to stimulate the immune system directly against tumor cells.)

"If the results of another recently completed phase 2 efficacy trial are also encouraging, the next step will be to compare this therapy head-to-head with the current standard of care," Chiocca says.

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The above story is reprinted from materials provided by Ohio State University Medical Center, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

E. A. Chiocca, L. K. Aguilar, S. D. Bell, B. Kaur, J. Hardcastle, R. Cavaliere, J. McGregor, S. Lo, A. Ray-Chaudhuri, A. Chakravarti, J. Grecula, H. Newton, K. S. Harris, R. G. Grossman, T. W. Trask, D. S. Baskin, C. Monterroso, A. G. Manzanera, E. Aguilar-Cordova, P. Z. New. Phase IB Study of Gene-Mediated Cytotoxic Immunotherapy Adjuvant to Up-Front Surgery and Intensive Timing Radiation for Malignant Glioma. Journal of Clinical Oncology, 2011; DOI: 10.1200/JCO.2011.35.5222

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Antiviral therapy associated with fewer recurring eye problems from herpes simplex virus

ScienceDaily (Sep. 13, 2010) — Taking oral antiviral medications following infection with the herpes simplex virus may be associated with a reduced risk of recurring eye-related manifestations of the disease, according to a report in the September issue of Archives of Ophthalmology, one of the JAMA/Archives journals.

"Herpes simplex virus (HSV) is a common cause of corneal disease and is the leading infectious cause of corneal blindness among developed nations," the authors write as background information in the article. After the initial exposure to the virus and the resulting systemic infection, herpes simplex establishes a latent infection in sensory nerve structures. Reactivation of this latent infection could lead to initial or recurrent disease in one or both eyes, including inflammation or infection of the cornea, eyelid, membrane inside the eye (conjunctivitis, or pink eye) or middle layer of the eye (uveitis).

Ryan C. Young, B.A., of Mayo Clinic, Rochester, Minn., and colleagues estimated the incidence of HSV eye disease in a community-based cohort, in Olmstead County, Minnesota, from 1976 through 2007. During this time period, 394 patients with ocular HSV were identified, for an annual incidence of 11.8 per 100,000 individuals.

Oral antiviral therapy was prescribed in 175 (44 percent) of these patients, who underwent therapy for an average of 2.8 years (36 percent of the average 7.7 years of follow-up). Patients not taking this prophylactic therapy were 9.4 times more likely to have a recurrence of epithelial keratitis (infection of the top layer of the cornea), 8.4 times more likely to have a recurrence of stromal keratitis (infection of deeper layers of the cornea) and 34.5 times more likely to have a recurrence of blepharitis (eyelid infection) or conjunctivitis than those taking antiviral medications.

A total of 20 patients experienced adverse outcomes, including visual loss and perforation of the cornea; of these, 17 (85 percent) were not taking oral antiviral prophylaxis.

"Overall, this community-based retrospective study demonstrated a stable incidence of HSV eye disease during a recent 32-year period," the authors write. "We found a more dramatic protective effect of oral antiviral prophylaxis on recurrences of ocular HSV than had been described previously."

"The results of this study suggest that oral antiviral prophylaxis should be considered for patients with frequent recurrences of corneal disease," they conclude. "Additionally, we recommend an evaluation of the possible barriers preventing compliance with antiviral prophylaxis and a reassessment of the cost-effectiveness of long-term oral antiviral therapy."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by JAMA and Archives Journals.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Ryan C. Young; David O. Hodge; Thomas J. Liesegang; Keith H. Baratz. Incidence, Recurrence, and Outcomes of Herpes Simplex Virus Eye Disease in Olmsted County, Minnesota, 1976-2007: The Effect of Oral Antiviral Prophylaxis. Arch Ophthalmol, 2010; 128 (9): 1178-1183 [link]

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Map of herpes virus protein suggests a new drug therapy

ScienceDaily (July 6, 2010) — The mechanism by which a herpes virus invades cells has remained a mystery to scientists seeking to thwart this family of viruses. New research funded by the National Institutes of Health and published online in advance of print in Nature Structural & Molecular Biology reveals the unusual structure of the protein complex that allows a herpes virus to invade cells. This detailed map of a key piece of the herpes virus "cell-entry machinery" gives scientists a new target for antiviral drugs.

"Most viruses need cell-entry proteins called fusogens in order to invade cells. We have known that the herpes virus fusogen does not act alone and that a complex of two other viral cell-entry proteins is always required. We expected that this complex was also a fusogen, but after determining the structure of this key protein complex, we found that it does not resemble other known fusogens," said senior author Ekaterina Heldwein, PhD, assistant professor in the molecular biology and microbiology department at Tufts University School of Medicine.

"This unexpected result leads us to believe that this protein complex is not a fusogen itself but that it regulates the fusogen. We also found that certain antibodies interfere with the ability of this protein complex to bind to the fusogen, evidence that antiviral drugs that target this interaction could prevent viral infection," Heldwein continued. Heldwein is also a member of the biochemistry and molecular microbiology program faculties at the Sackler School of Graduate Biomedical Sciences at Tufts.

"Katya Heldwein's work has resulted in a map of the protein complex needed to trigger herpes virus infection. The NIH Director's New Innovator Awards are designed to support such breakthroughs. This research not only adds to what we know about how herpes viruses infect mammalian cells, but also sets the stage for new therapeutics that restrict herpes virus's access to the cell," said Jeremy M. Berg, PhD, director of the National Institute of General Medical Sciences (NIGMS) at the National Institutes of Health.

"We hope that determining the structure of this essential piece of the herpes virus cell-entry machinery will help us answer some of the many questions about how herpes virus initiates infection. Knowing the structures of cell-entry proteins will help us find the best strategy for interfering with this pervasive family of viruses," said first author Tirumala K. Chowdary, PhD, a postdoctoral associate in the department of molecular biology and microbiology at TUSM and member of Heldwein's lab.

Currently, there is no cure for herpes viruses. Upon infection, the viruses remain in the body for life and can stay inactive for long periods of time. When active, however, different herpes viruses can cause cold sores, blindness, encephalitis, or cancers. More than half of Americans are infected with herpes simplex virus type 1 (HSV-1), which causes cold sores, by the time they reach their 20s. Currently, about one in six Americans is infected with herpes simplex virus type 2 (HSV-2), the virus responsible for genital herpes. Complications of HSV-2, a sexually-transmitted disease, include recurrent painful genital sores, psychological distress, and, if transmitted from mother to child, potentially fatal infections in newborn infants.

Heldwein teamed up with colleagues at University of Pennsylvania and used x-ray crystallography along with cell microscopy techniques to study the structure and function of this cell-entry protein complex in HSV-2. Heldwein is currently developing a molecular movie that illustrates how herpes virus enters the cell.

Additional authors are Tina Cairns, PhD, a research specialist; Doina Atanasiu, a research associate; and Gary Cohen, PhD, professor and chair, all in the department of microbiology at the University of Pennsylvania School of Dental Medicine; and Roselyn Eisenberg, PhD, professor in the department of microbiology at the University of Pennsylvania School of Veterinary Medicine.

This work was funded by the Office of the Director of the National Institutes of Health, through a New Innovator Award in 2007 to Ekaterina Heldwein. The New Innovator Awards, part of the NIH Roadmap for Medical Research initiative, are awarded to support early-career scientists who take innovative -- and potentially transformative -- approaches to major challenges in biomedical research. The work was also funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, and the Pew Scholar Program in Biomedical Sciences.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Tufts University, Health Sciences.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Tirumala K Chowdary, Tina M Cairns, Doina Atanasiu, Gary H Cohen, Roselyn J Eisenberg, Ekaterina E Heldwein. Crystal structure of the conserved herpesvirus fusion regulator complex gH-gL. Nature Structural & Molecular Biology, 2010; DOI: 10.1038/nsmb.1837

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Dating With Herpes - Do I Need to Take Suppressive Therapy?

When you come to terms with your herpes diagnosis, you'll really need to make a decision about what treatment options you will utilize. If you are single, and intend to date people without herpes - this is doubly important.

As you know, there is no cure to the herpes simplex virus. Although the virus is not deadly or particularly dangerous - it is still incurable. Disclosing your status to any potential sexual partner is a must. There are many within the herpes community who do not feel comfortable dating outside of the "group" - however when dating people who do not have herpes, there are a few things that you can and should do to protect them.

1. Be honest about your outbreaks: Nothing ruins spontaneity like an annoying herpes outbreak! You should consider yourself highly contagious when you are experiencing an outbreak, so it is best to refrain from intercourse during these times.

2. Pay attention to your prodrome symptoms: Part of being honest about your outbreaks involves you knowing when they actually occur. Due to the fact that they aren't always visible or noticeable - keep track of the symptoms you have immediately before an active outbreak. In other words, are your glands and lymph nodes tender? Do you have any body aches? Abnormal itching? A tingling sensation near your outbreak sites? Knowing your symptoms will give you a better idea of when you may be shedding.

3. Eat healthy: Many people with herpes report increase in outbreaks when they eat certain foods. It is widely known that things like peanuts, caffeine, and even wine can cause the dormant virus to make it's way to the surface. If certain foods are your triggers, try to avoid them or find alternatives.

4. Take a form of suppressive therapy: We're sure you've seen the cheesy Valtrex commercials - where one person in the couple has herpes, and the other person has not - and it's been that way for years! As cheesy as they may be, there is an element in truth behind the commercial and the product itself. Studies show that when taken regularly, Valtrex drastically reduces the chances of passing the virus on to your partner. If you are dating outside of the herpes community, you should make it a point to take your meds on a daily basis as prescribed.

5. Always use protection: It is important to note that the herpes simplex virus can be passed on even when you use condoms. Since the primary form of transmission is through skin to skin contact, if you have surface level shedding in a place not covered by a condom - you are still contagious. It is also important to remind you that both genital and oral herpes can be transmitted during oral sex. With those things said, using condoms is still a "must". Condoms combined with suppressive therapy reduce the transmission rate to less than 2-3%

Now these five tips are just a few of the ways to make dating those without herpes less stressful, the other alternative is to explore your dating options amongst the herpes community. Although the disease is still taboo and demonized, there is a rather large online dating community out there just waiting to meet you! Positive Singles is one of the premiere herpes dating sites.

Have you struggled with relationships since being diagnosed with genital herpes? Herpes doesn't signal the end of your love life. As managing editor of YouGotHerpes.com, I give practical tips and advice on how to have a fulfilling and meaningful love life after herpes.

Visit us today for your FREE E-BOOK on The Truth About Herpes Treatments and For the best tips on dating with herpes, visit us today at Herpes Dating Sites

http://www.YouGotHerpes.com

Yours In Health & Wellness!

Dating With Herpes - Do I Need to Take Suppressive Therapy?

When you come to terms with your herpes diagnosis, you'll really need to make a decision about what treatment options you will utilize. If you are single, and intend to date people without herpes - this is doubly important.

As you know, there is no cure to the herpes simplex virus. Although the virus is not deadly or particularly dangerous - it is still incurable. Disclosing your status to any potential sexual partner is a must. There are many within the herpes community who do not feel comfortable dating outside of the "group" - however when dating people who do not have herpes, there are a few things that you can and should do to protect them.

1. Be honest about your outbreaks: Nothing ruins spontaneity like an annoying herpes outbreak! You should consider yourself highly contagious when you are experiencing an outbreak, so it is best to refrain from intercourse during these times.

2. Pay attention to your prodrome symptoms: Part of being honest about your outbreaks involves you knowing when they actually occur. Due to the fact that they aren't always visible or noticeable - keep track of the symptoms you have immediately before an active outbreak. In other words, are your glands and lymph nodes tender? Do you have any body aches? Abnormal itching? A tingling sensation near your outbreak sites? Knowing your symptoms will give you a better idea of when you may be shedding.

3. Eat healthy: Many people with herpes report increase in outbreaks when they eat certain foods. It is widely known that things like peanuts, caffeine, and even wine can cause the dormant virus to make it's way to the surface. If certain foods are your triggers, try to avoid them or find alternatives.

4. Take a form of suppressive therapy: We're sure you've seen the cheesy Valtrex commercials - where one person in the couple has herpes, and the other person has not - and it's been that way for years! As cheesy as they may be, there is an element in truth behind the commercial and the product itself. Studies show that when taken regularly, Valtrex drastically reduces the chances of passing the virus on to your partner. If you are dating outside of the herpes community, you should make it a point to take your meds on a daily basis as prescribed.

5. Always use protection: It is important to note that the herpes simplex virus can be passed on even when you use condoms. Since the primary form of transmission is through skin to skin contact, if you have surface level shedding in a place not covered by a condom - you are still contagious. It is also important to remind you that both genital and oral herpes can be transmitted during oral sex. With those things said, using condoms is still a "must". Condoms combined with suppressive therapy reduce the transmission rate to less than 2-3%

Now these five tips are just a few of the ways to make dating those without herpes less stressful, the other alternative is to explore your dating options amongst the herpes community. Although the disease is still taboo and demonized, there is a rather large online dating community out there just waiting to meet you! Positive Singles is one of the premiere herpes dating sites.

Have you struggled with relationships since being diagnosed with genital herpes? Herpes doesn't signal the end of your love life. As managing editor of YouGotHerpes.com, I give practical tips and advice on how to have a fulfilling and meaningful love life after herpes.

Visit us today for your FREE E-BOOK on The Truth About Herpes Treatments and For the best tips on dating with herpes, visit us today at Herpes Dating Sites

http://www.YouGotHerpes.com

Yours In Health & Wellness!