herpes

Herpes may double the risk of developing dementia

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Scientists have found a link between herpes and dementia risk. istetiana/Getty Images

  • Anyone who has received a herpes diagnosis may be twice as likely to develop dementia than people who have not, according to a new study from Uppsala University in Sweden.
  • HSV-1, the type of the virus that causes cold sores or oral herpes, is most associated with the risk of dementia.
  • Nearly 80% of the adult population in Sweden and 57% to 80% of adults in the United States carries that type.

Anyone who has received a herpes diagnosis may be twice as likely to develop dementia than people who have not, according to a new study from Uppsala University in Sweden.

The study, which was published in the Journal of Alzheimer’s Disease, followed 1,000 70-year-old subjects for 15 years and confirmed previous research about the associations with the herpes virus and dementia.

Herpes results from infection with the herpes simplex virus (HSV), of which there are two types. Herpes simplex virus type 1 (HSV-1) causes oral herpes, affecting the mouth and surrounding skin but also potentially the genital region. Herpes simplex virus type 2 (HSV-2) typically causes genital herpes and is usually sexually transmitted. Nearly 572,000 people have HSV-2 infectionsTrusted Source each year, according to the Centers for Disease Control and Prevention (CDC).

Dementia is a wide term for cognitive decline disorders like Alzheimer’s disease and vascular dementia. It is associated with aging but is not a usual part of getting older.

Erika Vestin, a lead author of the study and a Ph.D. student at Uppsala University, told Medical News Today that the research confirms prior knowledge about the connections between dementia and herpes, but causality is still not concrete.

“We still do not have answers regarding causal mechanisms of this association, whether the virus causes the disease or if there is an indirect link,” Vestin said.

“Further, the association remains to be studied in different social and ethnic groups, and potential effects of herpes drugs on dementia risk need to be investigated in pharmaceutical drug studies,” she added.

How common is herpes and dementia?

According to the World Health Organization (WHO)Trusted Source, more than 55 million people worldwide have dementia and nearly 10 million more will receive a diagnosis of dementia each year. By 2030, it is estimated that the number of people with dementia will reach 78 million.

HSV, which remains for a person throughout their life, is quite common. According to the WHOTrusted Source, around 67% of people under age 50 globally have an HSV-1 infection, and 13% under age 50 have an HSV-2 infection., and 13% under age 50 have an HSV-2 infection. Most people with HSV-2 may not know they have it: Approximately 87.4%Trusted Source of people between the ages of 14 and 49 with genital herpes do not have a clinical diagnosis.

Up to 80% of the adult population in Sweden may have contracted HSV-1 at some point. The statistics are similar in the United States: 57% to 80% of adultsTrusted Source here have oral herpes.

The herpes virus causes sores or blisters in or around the mouth or genitals, alongside other symptoms. There is no cure for herpes, but treatment can help manage symptoms and reduce the likelihood of outbreaks recurring and transmission to partners.

What is the link between herpes and dementia?

Vestin said that the oral form of herpes is most likely the main factor in any connection between HSV and dementia, but that the virus itself can complicate those connections.

“The main culprit seems to be HSV-1, which commonly infects the oral region,” Vestin said. “However, HSV-1 and HSV-2 can both infect either the oral or the genital region, which is important to have in mind when these studies are conducted.”

Dr. Monica Gandhi, MPH, an infectious diseases specialist with the University of California, San Francisco, told MNT that the study does not prove causality.

“There could be important differences between those with or without herpes simplex virus (HSV) IgG status (past exposure) and those who developed dementia or not. It is difficult to control all confounders that have been traditionally associated with dementia (like diabetes, hypertension, history of stroke or myocardial infarction), and the authors state that their entire cohort had relatively low rates of these conditions,” Dr. Gandhi said.

“The authors did not find an association between treatment for HSV and dementia, which would be an interesting observation to see in another study if we wanted to be more convinced of a causal link,” Dr. Gandhi added.

“A good matched study where a group is matched on almost all possible confounders for dementia (hypertension, diabetes, smoking, other risk factors) to another group with the same risk factors but only one difference (HSV IgG status) could be helpful in providing further evidence,” she added.

Should I be worried if I have a herpes diagnosis?

Vestin suggested that getting diagnosed and treated with widely available drugs for the herpes virus would benefit anyone who does have it and indicated that previous research backs this.

“There are indications from large register studies that herpesvirus drug use may be associated with a decreased risk of dementia among symptomatic herpes simplex carriers. However, there are no pharmaceutical trials to confirm this. For now, herpes simplex carriers will have to rely on the same advice as the rest of the population, involving mainly lifestyle factors and cardiovascular health,” she said.

Dr. Gandhi said that the rates of herpes and dementia are different enough — and there are wildly divergent factors for any individual’s susceptibility — to warrant some caution around the study’s findings.

“The prevalence of HSV-1 and HSV-2 is very high in the population (up to 80%) and the rate of dementia is fortunately much lower. Traditional risk factors for strokes (which can induce dementia) include diabetes, hypertension and smoking, so keeping those factors controlled can be helpful for a person’s individual risk of dementia,” Dr. Gandhi said.

“Given how common herpes virus infection is [in] young people, I would not let this study concern you too much,” she added.

Herpes’ Achilles’ Heel

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In a first, scientists use gene editing to disrupt both latent and active herpesvirus in human cells

microscopy image of herpes simplex virus

Scientists have used gene editing to disrupt both latent and actively replicating herpes simplex virus in human cells.
The herpes simplex virus, commonly known as the cold sore virus, is a devious microbe.

It enters the body through regions lined with mucous membranes—mouth, nose and genitals—but quickly establishes lifelong viral hideouts inside nerve cells.

After initial infection, the virus lurks dormant only to be reawakened periodically to cause outbreaks marked by the eruption of cold sores or blisters. In a handful of people, the consequences of viral reawakening can be devastating, including blindness and brain inflammation.

Antiviral medications can prevent recurrent outbreaks, but they are not always effective, so for decades, researchers have sought a solution that would quiet the virus for good.

Now, using human fibroblast cells infected with herpes simplex virus (HSV), researchers at Harvard Medical School have successfully used CRISPR-Cas9 gene editing to disrupt not only actively replicating virus but also the far-harder to reach dormant pools of the virus, demonstrating a possible strategy for achieving permanent viral control.

The team’s findings are described Dec. 2 in eLife.

“This is an exciting first step—one that suggests it is possible to permanently silence lifelong infections—but much more work remains to be done,” said study lead investigator David Knipe, the Higgins Professor of Microbiology and Molecular Genetics in the Blavatnik Institute at Harvard Medical School.

Notably, the research represents the first successful instance of disrupting latent viral reservoirs through gene editing. Latent reservoirs are notoriously impervious to antiviral medications and have also proven hard to gene-edit.

The experiments also identify the mechanisms by which actively replicating virus becomes uniquely vulnerable to gene editing. These very mechanisms may also explain why latent forms of the virus are less amenable to this technique.

Specifically, the experiments reveal that the DNA of an actively replicating virus is more exposed to the Cas9 enzyme—the molecular scissors in the CRISPR-Cas9 gene-editing system. This is because actively replicating viruses have fewer protective histones that wrap around their DNA to shield it.

“The absence of protective histones makes the DNA more accessible and easier to cut, so it’s essentially identified HSV’s Achilles heel,” Knipe said.

A model system

The new findings offer a model system for using gene editing in a localized way to disrupt active replication in specific sites. However, Knipe cautions, the arch-challenge of delivering gene-editing therapy to neurons—where the virus hides and enters a state of dormancy—remains to be solved, Knipe added.

More than two-thirds of the world population harbors the virus according to the World Health Organization. While most infections are asymptomatic, in a handful of people HSV can cause serious damage. It can infect the eyes, a condition known as herpes keratitis, and lead to blindness. In people with compromised immune systems, HSV can cause brain inflammation. In newborns, the virus can cause disseminated, systemic disease and brain inflammation and can be fatal in a quarter of infected babies.

Thus, one early therapeutic use of this technique could involve local and limited gene-editing of the epithelial cells in the mouth, eyes or genitals of people with established HSV infections as a way to prevent the virus from causing active outbreaks at vulnerable sites, Knipe said.

“If you want to prevent corneal infections, for example, you might be able to use CRISPR-Cas9 editing in the corneal cells to prevent new infections or prevent the virus from reactivating or reduce the reactivation,” Knipe said. “People who have recurrent herpes keratitis infection of the cornea start to go blind after a while because of the reactivation and the resulting inflammation that causes clouding of the cornea.”

The advantage of limited, localized gene-editing is avoiding the widespread, possible off-target effects that might inadvertently alter the DNA of cells other than those intended.

“We still have a long way to go in ensuring hyperprecision and safety of new gene-editing tools so local editing could offer a safer, more limited first step,” Knipe said.

How the Immune System Fights to Keep Herpes at Bay

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New study findings could inform the design of treatments for a range of viruses that replicate in the cell nucleus

Two oval-shaped objects made up of glowing green dots float in a black field. The object on the left has fewer glowing dots than the object on the right.

These microscope images show how interferon in the nucleus raises levels of the protective protein IFI16 (stained green) from low background levels (left) to the higher levels needed to resist herpes infection (right).


At a glance:

  • In a study of lab-engineered cells, Harvard Med researchers identify how the immune system neutralizes the herpesvirus.
  • The research maps, for the first time, the maneuvers used by virus and host in the cell nucleus, a poorly understood terrain of host-pathogen interaction.
  • The findings could inform the design of new treatments for herpes and other viruses that replicate in the same way.

Herpes simplex virus (HSV) is extremely common, affecting nearly two-thirds of the world’s population, according to the World Health Organization.

Once inside the body, HSV establishes a latent infection that periodically awakens, causing painful blisters on the skin, typically around the nose and mouth. While a mere nuisance for most people, HSV can also lead to dangerous eye infections and brain inflammation in some people and cause life-threatening infections in newborns.

Researchers have long known that the virus and the host immune system are in a perpetual competition, but why does this battle reach a stasis in most people while causing serious infections in others?

More important, precisely how does the battle unfold at the level of cells and molecules? This question has continued to bedevil scientists and hamper the quest for treatments that prevent or cure infections.

A recent study by researchers at Harvard Medical School, conducted using lab-engineered cells and published in PNAS, unveils the precise maneuvers used by host and pathogen in the fight for dominance of the cell.

Furthermore, the research shows how the immune system keeps the virus at bay in a battle taking place at the control center of the cell — its nucleus.

Immune signaling proteins issue a call to arms

The research reveals a key role for a group of signaling proteins called interferons, which recruit other protective molecules and block the virus from establishing infection.

Once inside the host, HSV multiplies by making copies of itself inside the nuclei of cells, using the host’s genetic machinery. For that to happen, the virus must outcompete the host’s immune system. But many of the tactics the virus and the immune system use in this contest have remained a mystery, making it challenging to design medicines to help patients defeat the virus.

Interferons — named for their ability to interfere with pathogens’ attempts to infect cells — are signaling molecules released when the immune system detects the presence of microbes, such as viruses. The distress signals sent by interferons activate genes in that cell and other cells that produce proteins, which in turn block viruses from establishing infection in the first place.

Several different mechanisms that interferons use to thwart viruses within the cytoplasm, the gelatinous liquid that fills cells, are well known. But how interferons work against DNA viruses — those launching their attack within the cell nucleus — has remained elusive.

“We know a lot about how interferon and immune stimulants work against viruses in the cytoplasmic body of the cell, but up until now, we knew very little about how the immune system blocks viral infection in the cell’s nucleus,” said study senior author David Knipe, the Higgins Professor of Microbiology and Molecular Genetics in the Blavatnik Institute at HMS. “Our findings define the mechanisms of action of any treatment that induces interferons and how they can prevent and treat infections from HSV, as well as other herpesviruses and nuclear DNA viruses.”

Knipe said the insights from this work could also help researchers understand — and perhaps eventually develop treatments for — other nuclear DNA viruses, including well-known troublemakers like the Epstein-Barr virus, which causes mononucleosis; human papillomavirus; hepatitis B; and smallpox.

These results define the mechanisms of action of interferon treatments for herpesvirus diseases and other treatments such as toll-like receptor ligands that have been tested for herpes, the researchers said. Other new activators of interferons such as cGAS agonists could also be used to induce herpes resistance through the newly defined mechanisms, the researchers added.

The researchers caution that any new potential therapies for HSV and other DNA viruses are purely conceptual at this point. Any such approaches should be first tested in small animals such as mice, then in larger animals and, finally, in humans.

Mapping the steps of a viral arms race

In the new study, Knipe and co-author Catherine Sodroski, an HMS PhD graduate now at the National Institutes of Health, discovered that a host protein called IFI16 is recruited by interferon to help block the virus from reproducing in several ways.

One of the strategies used by IFI16 to fend off HSV involves building and maintaining a shell of molecules around the viral DNA genome. This molecular “bubble wrap” prevents the virus from unfurling. With the virus wrapped up, it can’t activate its DNA to express its genes and make copies of itself.

To counter these protective maneuvers, however, the virus produces molecules called VP16 and ICP0 that can remove the wrapping, deactivate the host cell’s protective molecules, and enable the virus to reproduce.

Another mechanism used by IFI16 to fight HSV infection is to neutralize VP16 and ICP016. Under normal circumstances, when the cell is not preparing to repel a viral invader, there is some IFI16 present within the nucleus. But this background level of IFI16 isn’t enough to fight off the viral helper proteins and keep the virus wrapped and restrained.

Without interferon’s call to the cell to send in more IFI16, the virus wins the arms race and infects the cell. However, the experiments showed, when interferon signals recruit higher levels of IFI16, the immune system wins.

This current study echoes similar findings that found elevated levels of IFI16 in clinical samples of tissues where the immune system appeared to be successfully controlling symptoms of the closely related HSV-2 virus, providing crucial insights about the molecular machinery at work in staving off outbreaks of symptoms.

Using insights from the lab to improve human health

Knipe says he became interested in the biology of herpesviruses as an undergraduate while recovering from a bout of mononucleosis. He turned that curiosity into a career.

The Knipe lab studies what happens at the level of molecules and cells when HSV causes symptomatic and dormant infections. He is particularly interested in how the host immune system responds to HSV. Knipe has applied the insights gained by studying HSV to explore the possibilities of using genetic material from HSV to deliver vaccines for HIV, SARS, West Nile, and anthrax.

“Solving the puzzles that underlie the basic biology of how these viruses interact with the host cell nucleus and immune system is endlessly fascinating, and finding new ways to apply that knowledge to fighting diseases is endlessly rewarding,” Knipe said. “The most exciting part is that we’re just scratching the surface of the deep knowledge we can tap into for this fight.”

12 Preventable STDs: Pictures, Symptoms, Diagnosis, Treatment

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Are you prepared to protect your health from sexually transmitted diseases and infections?

Are you prepared to protect your health from sexually transmitted diseases and infections? Some of these infections are more familiar—you’ve probably heard of chlamydia, gonorrhea, genital herpes, and HIV. But many more are less talked about. You can protect yourself and your loved ones from future health problems by understanding these common STDs.

In this article we answer some of your tricky and sometimes uncomfortable questions about STD symptoms and diseases. You will learn why herpes is sometimes considered a sexually transmitted disease, what sexual disease is nicknamed “the clap,” and which kinds of infection can lie dormant for a long time. You will also find information on the best treatments for herpes, HIV, chlamydia and various other sexually-transmitted diseases.

STD or STI?

Some experts prefer the term “STI” (sexually transmitted infection). STIs include all infections that can be transmitted sexually.

Genital Warts (HPV)

Are you prepared to protect your health from sexually transmitted diseases and infections?

It’s not necessary to have sexual intercourse for a sexually-transmitted disease (STD) to harm your health. The human papillomavirus (HPV), the disease that causes genital warts, can be transmitted by close skin-to-skin contact. Some types of HPV cause cervical or anal cancer, and vaccines are available to protect against the most dangerous types. Other HPV types cause genital warts, which can be raised, flat, or cauliflower-shaped. HPV can be transmitted even by people who have no visible warts or other symptoms.

HPV Symptoms

Genital warts can be big or small, flat or raised. They generally appear as a small bump or group of bumps in the genital region, and may be shaped like a cauliflower.

HPV Vaccine

A vaccine to prevent HPV is given in three shots. The second shot is given a month or two after the first shot. The third shot comes six months after the first shot.

The Centers for Disease Control recommends boys and girls be vaccinated at ages 11 or 12.

If they did not get the HPV vaccine as children, women can get the HPV vaccine through age 26. Men can get it through age 21. The CDC recommends HPV vaccination for men through age 26 for men who have sex with men or men with compromised immune systems, including HIV.

Pubic Lice (Crabs STD)

This name refers to the shape of these parasites, which is different from that of body lice.

Pubic lice are colloquially known as “crabs.” This name refers to the shape of these sexually-transmitted parasites, which is different from that of body lice. Pubic lice live in pubic hair and are spread among people during close contact. Pubic lice can be treated with over-the-counter lice-killing medications.

Pubic Lice (Crabs) Symptoms

  • Severe itching
  • Visible crawling lice or eggs attached to pubic hair

Scabies

Scabies is often spread during sexual contact.

Do you know what scabies infections look like? Like pubic lice, scabies are another parasitic STI. This parasite is not necessarily sexually transmitted, since it can affect any area of the skin. However, scabies may be spread during sexual contact.

Scabies Symptoms

  • Extreme itching that is worse at night.
  • The skin appears to have a pimple-like rash, as shown in the above photo.
  • Both the itching and rash may be across the body or limited to the wrist, elbow, armpit, webbing between fingers, nipple, penis, waist, belt-line or buttocks.
  • Tiny blisters (vesicles) and scales may appear.
  • Tiny burrows left by the tunneling of female scabies mites may be visible on the skin. They appear as tiny raised and crooked grayish-white or skin-colored lines.

The only way to prevent this STI is to avoid touching people, as any skin-to-skin contact can spread this highly contagious mite. Condoms, while good at preventing many diseases, will not prevent scabies.

Fortunately, this STI is treatable. Prescription creams can cure a scabies infestation. Protect your health by visiting a doctor if you believe you may have this STI.

Gonorrhea (The Clap)

Gonorrhea is easily transmitted.

Gonorrhea is an easily transmitted disease that affects both men and women. The disease is also termed “the Clap” from the French word for brothel (clapier) and the early treatment of gonorrhea by clapping both hands against the penis or using a heavy object (like a mallet) on the penis to squeeze out pus in the penis (note, these old treatments are not recommended because they can damage the penis and they do not cure the disease). It can harm your health by causing infertility in men and women if it is left untreated. There may be no early symptoms of this common STD. This is what a gonorrhea infection looks like.

Gonorrhea Symptoms

  • Burning during urination
  • Vaginal or urethral discharge
  • Pelvic pain in women
  • Men may experience swelling of the testes and discharge from the penis

In some cases, the symptoms are mild and the condition is mistaken for a UTI or yeast infection. Visit your health care provider if this sounds like your symptoms.

Syphilis

Syphilis can be cured with antibiotics.

Have you seen a syphilis infection? Syphilis can be cured with antibiotics, but many people don’t notice its early STD symptoms. It can play havoc with your health, leading to nerve damage, blindness, paralysis, and even death over time if not treated.

Syphilis Symptoms

  • A round, firm, painless sore on the genitals or anal area (often the first sign)
  • A rash can develop later on the soles of the feet, palms, or other parts of the body
  • Enlarged lymph nodes
  • Fever
  • Fatigue
  • Hair loss
  • Late-stage syphilis can cause damage to many different organ systems. That’s why early detection is so critical to your health.

Chlamydia

Chlamydia is a very common STD.

Chlamydia is a very common STD. It can cause infertility if not treated. The symptoms may not be noticed, or they may be vague and nonspecific. Some people experience no health effects at all.

Chlamydia Symptoms

  • Burning or itching of the genitals
  • Discharge
  • Painful urination

Chlamydia infections can also develop in the rectum and throat.

Oral Herpes (Herpes Simplex 1 Virus)

Oral herpes is usually not considered a sexually transmitted disease.

This is what oral herpes looks like. Cold sores or “fever blisters” on the lips are a sign of herpes virus infection, usually caused by the type of herpes virus known as human herpes virus 1, also known as oral herpes.

Oral herpes is usually not considered a sexually transmitted disease. It can be transmitted through kissing or household contact. However, it can also spread to the genitals. (While this type of herpes can be contracted on the genitals, it is different from the disease known as genital herpes). There is no cure for herpes infection, but medications can reduce the severity and duration of outbreaks.

Oral Herpes

  • Itching of the lips or skin around the mouth
  • Burning near the lips or mouth area
  • Tingling near the lips or mouth area
  • Sore throat
  • Swollen glands
  • Painful swallowing
  • A rash may form on your gums, lips, mouth or throat

Symptoms of oral herpes usually appear 1-3 weeks after first infection. When symptoms return, they are typically milder than the initial herpes outbreak.

Genital Herpes (Herpes Simplex 2 Virus)

As with oral herpes, medications can reduce the severity of genital herpes, but there is no cure.

In contrast to oral herpes, genital herpes infections are caused by a different virus known as HSV-2 or HHV-2. The genital herpes virus spreads through direct genital contact and is considered an STD. More than 87% of those infected with genital herpes are unaware of their infection due to very mild or nonexistent symptoms.

Genital Herpes Symptoms

  • Painful, fluid-filled blisters and crusted sores on the genital area, buttocks, thighs, or anus.
  • Mild tingling or shooting pain in the legs, hips, or buttocks may occur hours to days before a genital herpes outbreak.

After the first infection, less severe outbreaks are common in the first year. Outbreaks tend to decrease over time, though the infection may stay in the body indefinitely.

A genital herpes infection can spread to the lips through oral contact. As with oral herpes, medications can reduce the severity of genital herpes, but there is no cure.

Hepatitis B

Hepatitis B is a virus that spreads through contact with body fluids and blood, so it can be transmitted through sexual intercourse.

Hepatitis B is a virus that spreads through contact with body fluids and blood, so it can be transmitted through sexual intercourse. Hepatitis B infection is also possible through sharing of needles, razors, and toothbrushes. Babies can become infected at birth from an infected mother. It’s possible to go for years without symptoms of this STI.

Hepatitis B Symptoms

  • Nausea
  • Abdominal pain
  • Jaundice (yellowing of the skin and whites of the eyes)
  • Over time, scarring of the liver (cirrhosis) and liver cancer can develop.

Although there is no cure, there is a vaccine to help prevent hepatitis B infection.

HIV/AIDS

The HIV virus (AIDS virus) weakens the body's immune system.

The HIV virus (AIDS virus) weakens your body’s immune system. It is spread through sexual contact, needle sharing, or from an infected mother to her baby. There may be no symptoms for years, but a blood test can tell if you have been infected. With appropriate treatment, many serious illnesses can be prevented.

HIV Symptoms

  • Flu-like symptoms 1 to 2 months after first infection, including like swollen lymph nodes, fever, and headaches
  • Chills
  • Rash
  • Night sweats
  • Sore throat
  • Swollen lymph nodes
  • Mouth ulcers

AIDS Symptoms

  • Rapid weight loss
  • Recurring fever or profuse night sweats
  • Extreme and unexplained tiredness
  • Prolonged swelling of the lymph glands in the armpits, groin, or neck
  • Diarrhea that lasts for more than a week
  • Sores of the mouth, anus, or genitals
  • Pneumonia
  • Red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelids
  • Memory loss, depression, and other neurologic disorders

HIV Testing

There are accurate tests to identify whether or not you have been infected with the HIV virus.

Want to know about HIV testing? There are accurate tests to identify whether or not you have been infected with the HIV virus. These can be done in the clinic or at home with the FDA-approved Home Access test kit. The test can be performed anonymously, with only a number to identify you. However, sometimes people may not test positive in the initial 3-4 weeks to 6 months after infection. This time period is referred to as the “window period” in which antibodies may not have developed enough for a positive test. You can still transmit the virus to others during this time.

HIV/AIDS Treatment Options

While there is no cure for HIV, there are medications that can suppress the amount of virus multiplying inside the body.

While there is no cure for HIV, there are medications that can suppress the amount of virus multiplying inside the body. People take a combination of antiviral drugs in hopes of preventing the infection from advancing to AIDS. Additional treatments can help prevent or fight off serious infections, if the immune system has weakened. While there is no cure for HIV/AIDS, there are highly effective prophylactic (PrEP and PEP) medications that can dramatically reduce a person’s risk. Ask your doctor for more information about PrEP and PEP medications.

Trichomoniasis (“Trich”)

Most affected men have no specific symptoms of trichomoniasis.

Trichomoniasis is a parasitic infection (caused by Trichomonas vaginalis) that is spread during sexual contact. It affects both men and women and can be cured with medications. Most affected men have no specific symptoms.

Trichomoniasis Symptoms

  • Men: minor discharge or burning with urination
  • Women: yellowish-green vaginal discharge with a prominent odor, itching of the vaginal area, or painful sex or urination

Symptoms can develop anywhere from 5 to 28 days after contracting the infection.

Chancroid

Chancroid is more common in Africa and Asia.

Chancroid is an STD that is rarely seen in the U.S. It is more common in Africa and Asia. It causes painful lumps in the genital area that can progress to open sores. Antibiotics can cure the infection; chancroid is caused by bacterial infection with Haemophilus ducreyi.

Chancroid Symptoms

  • One or more sores or raised bumps on the genitals. A narrow, red border surrounds the sores. The sores become filled with pus and eventually rupture into a painful open sore.
  • About half the time when untreated, the chancroid bacterial infection spreads to the groin’s lymph glands, causing the groin to enlarge and become hard and painful.

Lymphogranuloma venereum (LGV)

Like other chlamydial infections, LGV can be cured by antibiotic treatment.

Lymphogranuloma venereum (LGV) is a type of chlamydial infection, but it is caused by a different type of chlamydia (Chlamydia trachomatis) than the usual chlamydial disease. Like other chlamydial infections, it can be cured by antibiotic treatment.

Early Lymphogranuloma venereum Symptoms (3-12 Days After Exposure)

  • Soft red, painless sores on or near the genitals or anus
  • Similar sores in the throat or mouth following oral sex

Later Lymphogranuloma venereum Symptoms (2-6 Weeks After Exposure)

  • Open sores in the genitals
  • Swollen lymph nodes in the groin
  • Headache
  • Anal sores and rectal discharge or bleeding if the infection was acquired through anal sex
  • Painful urination
  • Constipation
  • Rectal bleeding
  • Pain in lower back/abdomen
  • Pus-filled or bloody diarrhea
  • Fever, chills, joint pain, decreased appetite and fatigue

Pelvic Inflammatory Disease

In PID, bacteria spread to the uterus and female reproductive tract.

Pelvic inflammatory disease (PID) is not a specific STD. Rather, it is a complication that can develop from various diseases, particularly gonorrhea and chlamydia. In PID, bacteria spread to the uterus and female reproductive tract. Infertility may result if the condition is not treated right away.

Pelvic Inflammatory Disease Symptoms

  • Fever
  • Pelvic or low abdominal pain
  • Painful urination
  • Discharge
  • Painful intercourse
  • Light bleeding

Who’s at Risk of Sexually Transmitted Diseases?

About half of sexually active young adults acquire at least one of these diseases by age 25.

It’s estimated that half of sexually active young adults acquire at least one of these STIs by age 25. In fact, sexual diseases are the most commonly reported type of infection in America. Though more common in teens and young adults, anyone who is sexually active is potentially at risk. The risk is raised by having multiple sex partners. The incidence of some sexually transmitted diseases, including LGV and syphilis, is increasing in men who have sex with men.

Can Virgins Get Sexually Transmitted Diseases?

Many of these diseases can spread through any type of sexual activity.

Many of these diseases can spread through any type of sexual activity. This can include skin-to-skin contact and oral sex. This means that people who have not yet had sexual intercourse can still get infected.

Preventing Infection

Abstinence from any sexual contact is the only absolute way to prevent STIs.

Abstinence from any sexual contact (or skin-to-skin contact) is the only absolute way to prevent STIs. Being in a long-term, monogamous relationship also is a good way to avoid them.

There are also steps you can take to decrease the chance of getting an STD if you are sexually active, including:

  • Asking partners if they have ever been infected.
  • Using condoms.
  • Avoiding sexual activity with a partner who shows STD symptoms.
  • Asking partners to be tested before having sex.
  • Being aware of symptoms and signs of these conditions.

The Limits of Condoms

Condoms can prevent the spread of some STDs.

Condoms can prevent the spread of some STDs, but they aren’t 100% effective. They are less effective at protecting against herpes, syphilis, and genital warts, since these STDs can be transmitted by contact with skin lesions that are not covered by a condom. Condoms also do not protect against crabs and scabies infestations.

How to Tell Your Partner You Are Infected

Tell your partner as soon as possible if you believe you may be infected.

It may be difficult, but it is important to tell your partner as soon as possible if you believe you may be infected. Even if you are being treated, you may still be able to spread the infection. For some diseases, both partners should be treated at the same time.

It can be difficult to share this information, so some people find that preparing a script in advance can be helpful. Here are some facts that can help the conversation go more smoothly:

  • Discovering a sexually transmitted disease is not necessarily evidence of cheating. It may very well have come from either your past relationship or that of your partner.
  • An estimated one in two sexually active people will contract such a condition by the time they reach age 25. Most of these don’t know they have an infection. Many STD symptoms are subtle or don’t even show up when first contracted and may be discovered much later.

It’s normal to be nervous about this topic. But by being bold and taking action, you can actively promote better health for you and your partner.

STDs and Pregnancy

Some STDs can cause premature labor in pregnant women.

Some STDs can cause premature labor in pregnant women, and many STDs can be passed to the baby either during pregnancy or childbirth. So, all pregnant women should be checked for STDs. STDs can cause numerous problems in babies, like low birth weight, stillbirth, nerve problems, blindness, serious infections, and liver problems. Treatment during pregnancy can reduce the risks of these complications and can cure many types of infections.

Can STDs Come Back?

Most treatments don't protect you from developing the STD at a future time.

In most cases, new exposures to STDs that you have already acquired in the past can cause you to get the infection again. Most treatments don’t protect you from developing the STD at a future time. If your partner has not been treated, you may pass the infection back and forth. Without the right precautions, you could acquire a second STD or a recurrence of the same infection. In addition, genital herpes virus infections can be recurrent after a single exposure.

How to Get Tested for Herpes

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Testing for herpes and other types of sexually transmitted diseases is important, but how do you know which test you should take? The American Sexual Health Association (ASHA) has a handy infographic that you can use as a reference, especially if you or someone you know may have herpes.1

herpes testing

Story at-a-glance

  • If you observe symptoms of herpes such as lesions or sores, take a herpes viral culture of lesion or a swab test of the sores within the first 48 hours after these become visible
  • Testing for herpes and other types of sexually transmitted diseases is important, but how do you know which test you should take?

Undergo a Herpes Viral Culture of Lesions Test

If you observe symptoms of herpes such as lesions or sores,2 take a herpes viral culture of lesion or a swab test of the sores3 within the first 48 hours after these become visible. In about a week, you will receive your results and know if you have herpes or not.4

According to ASHA, this herpes viral culture of lesion has a major pro and con. The test is typically known for its accuracy in generating a positive result — if you test positive for herpes, you can be certain that you have the virus. Moreover, the test is also able to classify if the infection is caused by the HSV-1 or HSV-2 virus.5

However, you should be aware that a herpes viral culture of lesion turns in a high rate of false negatives. This culture test needs an active virus, and if the sample you obtained is very small or is already starting to heal, there is a reduced possibility of getting an accurate culture.6

The amount of hours after a lesion first appears is also a factor — you might receive a false negative if you take a test more than 48 hours after these symptoms first appear. What’s more, if you get a herpes viral culture of lesion on your second herpes outbreak, the result may be less accurate.7

A NAAT Test Can Check If You Have Herpes or Not

Apart from a swab test, a Nucleic Acid Amplification Testing (NAAT) can also be performed to check for herpes. Because of its speed and accuracy to determine if a patient has an HSV-1 or HSV-2 virus, as well as its lower risk to yield a false negative result, NAATs are the preferred method in examining herpes cases.

Polymerase Chain Reaction or PCR tests are the most widely-used NAAT method. This test determines DNA from the virus and categorizes if it’s either the HSV-1 or HSV-2 virus. Your physician will recommend a PCR test for you if there’s active viral shedding.

This test is usually performed on cells or fluids from a sore, on blood or other bodily fluids (such as the spinal fluid).8

PCR tests are also known for their accuracy because they produce multiple copies of the viral genetic material in four hours, so even just a small amount of the virus can diagnose herpes. Unfortunately, PCR tests are both expensive and not widely available, so you might have to search extensively for a physician who can perform this type of test.9

If you don’t feel any symptoms but decide to have yourself checked anyway, your physician will first do a visual examination of the visible sores. Sometimes, a laboratory test may also be performed, but it’s not always necessary.

Ask About Antibody or Blood Tests as Well

You can also ask your physician to perform an antibody or blood test, since it could find the herpes simplex virus even before an outbreak occurs.10,11 This blood test is supposed to search for immunoglobulin (IgG) antibodies, which can be further broken down to know which of the two viruses cause a case of herpes.

While this antibody test is known for its accuracy, the periods when the IgG antibodies can be detected are different from person to person. Someone may have detectable IgG antibody levels in just weeks, but another person may have these levels in months. If a patient takes this test too long after he or she gets the virus, there’s a chance that the test will yield a false negative.12

ASHA advises to wait for at least 12 to 16 weeks from the final possible date of exposure before undergoing a type-specific blood test to ensure that the antibodies can be fully detected.13

You can avail of various FDA-approved and IgG-based blood tests that can show if you have herpes or not. They don’t discover if the infection site is oral or genital in nature, but they do provide accurate results. For example, as most cases of genital herpes are triggered by the HSV-2 virus, if you get a positive result for type-2 antibodies, you most likely have genital herpes

Doctors Warn Herpes Could Cause Alzheimer’s Disease

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Why Is This Important?

Because herpes might be more than an unsightly inconvenience.

Long Story Short

An editorial written by experts in the study of Alzheimer’s disease insist there is enough research to suggest a possible connection between the disease and two common STDs, as well as a particular bacteria. Their editorial is an urgent call to action to start trials using microbial therapy.

Long Story

Alzheimer’s is a terrible way to end a life. Loved ones die alone, robbed of rich memories with no recognition of the loving faces around them.

In simple terms, the disease is caused by brain cell death. Genetic factors play a role in who develops Alzheimer’s and environmental variables are regarded as a contributing factor but — as much as this plainly sucks for anyone keen to live a long life — the major established risk factor remains advanced age.

Science is desperately trying to find a cure for the neurodegenerative disease, along with a means to prevent its onset or, at the very least, slow its progression. Seemingly promising drug trials have fallen flat, leaving researchers empty-handed.

Brains. Lots of brains.

Now they may have a new direction.

Established scientists, researchers and clinicians have just published an editorial in the Journal of Alzheimer’s Disease. They are calling for urgent examination of the link between Alzheimer’s and two sexually transmitted diseases.

The 31 experts who contributed to the editorial warn the herpes virus may be a cause of Alzheimer’s. They also identify the chlamydia bacteria as another possible cause, as well as a bacteria called spirochaete.

They insist huge amounts of research and evidence already point to certain microbes as the cause of Alzheimer’s disease.

One of the scientists, Professor Douglas Kell of the University of Manchester’s School of Chemistry, says, “There is incontrovertible evidence that Alzheimer’s disease has a dormant microbial component. We can’t keep ignoring all of the evidence.”

Basically, the experts believe some sort of destructive microbe, bacteria or germ gets into the brain and curls up for a nap. Then, as time goes by and the immune system is compromised, the microbe wakes up and begins to inflict its damage.

The scientists are focused particularly on herpes simplex virus type 1 (HSV-1). Shockingly, most people get this particular strain of virus as a child, whereas herpes simplex type 2 (HSV-2) is transmitted through sexual contact.

What’s particularly gnarly about HSV-1 is that a carrier can give it to anyone else by simply touching their skin, sharing silverware or lip balm.

An estimated two thirds of people are believed to have been infected by the herpes virus and many of them never realize they have it.

In the US, one out of every six people between the ages of 14 and 49 has genital herpes.

According to last year’s figures, 47.5 million people around the world are living with dementia brought on by diseases like Alzheimer’s, and that number will rise to 75.6 million in 2030, and then triple to 135.5 million by 2050.

About 5.3 million Americans of all ages have Alzheimer’s disease.

The Director of Research at Alzheimer’s Research UK, Dr Simon Ridley, says, “…there isn’t conclusive evidence to suggest that a particular infectious agent or microbe could be directly responsible for causing the disease.” He goes on to emphasize, “There is no evidence that Alzheimer’s can be passed from person to person like a virus.”

For a while, science was focused on the aluminum we eat and breathe as a possible cause of Alzheimer’s disease, but conflicting findings have convinced most researchers to leave it alone.

There has also been work suggesting an environmental toxin in seafood might be a cause.

Given the prevalence of both Alzheimer’s disease and herpes, there is, clearly, no time to waste. The editorial is an urgent call to action, with the authors recommending studies using antimicrobial therapy. They suggest new findings could have implications for other progressive neurological conditions.

Scientists are using herpes to treat skin cancer .

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In a few months time, those suffering from skin cancer may find an unlikely hero in their treatment regimen: herpes. A modified version of the Herpes Simplex 1 virus (known for causing cold sores and some cases of genital herpes) called T-Vec has successfully been used to treat melanoma in a phase III clinical trial. That means it’s just waiting for a final okay from the FDA before the Amgen product can hit the market. The results of the trial were published Tuesday in Journal of Clinical Oncology.

In a study of 436 patients with inoperable melanoma, Talimogene Laherparepvec had 16.3 percent of patients showing results at the six-month mark, compared to 2.1 percent taking the control therapy. Some patients were continuing to respond to T-VEC three years later.

Patients with stage III and early stage IV melanoma treated with T-VEC (163 people in all) lived an average of 41 months. This compared with an average survival of 21.5 months in the 66 earlier-stage patients who received the control immunotherapy. Immunotherapy, where agents are used to boost a body’s natural defense against a tumor, are already the best treatments against melanoma. But this is the first time a modified virus has been successful in carrying out that treatment.

Using a virus as a drug isn’t a new idea. Phage therapy, where viruses that attack certain bacteria are used in place of antibiotics, is commonly used in Europe and on the rise in the United States. But cancer therapies like the one described in the new paper take things a step further, manipulating existing viruses to turn them into cancer-fighting tools.

Kevin Harrington, Professor of Biological Cancer Therapies at The Institute of Cancer Research and head of the trial, has been working on this particular virus for about a decade. Before he signed onto the project, it was primarily being investigated as a breast cancer treatment. But Harrington brought head, neck, and skin cancer patients into the mix, and melanoma seemed to have the best responses of all.

Here’s how T-VEC works: It starts with the herpes virus, which is magnificent at proliferating itself within cells and then causing them to burst (that’s where the cold sores come from). But T-VEC has had two key genes removed. These keep it from replicating within healthy cells, which can quickly spot it because of the missing genes.

 

But cancer cells aren’t as savvy, and T-VEC has its run of them. Meanwhile, T-VEC has also been modified to produce a molecule called GM-CSF, which serves as a red flag waved at the immune system.

So in addition to the destructive power of the T-VEC cells themselves, the therapy summons the immune system right to where it’s needed — the tumor.

“This is a first in class agent, a brand new therapy,” Harrington said. “But it’s just the farthest along of what we hope will be many more.”

Harrington expects the FDA to clear T-VEC within the year, and it could potentially be available to patients right away.

But there’s more work to be done to determine just how T-VEC can fit into the cancer-treatment landscape. When the latest trial was started, Harrington explained, there was no standard of treatment for melanoma — so it’s compared to a treatment that no one expected to outpace T-VEC. Now that other therapies  — ones that target specific mutations in patients’ cancer cells — are showing more success than what was available when the trial was formed, researchers will have to see how T-VEC compares.

“The next steps are exciting, and already underway,” he said. “The next big frontier will be to combine this with existing immunotherapies. There’s a strong rationale that other drugs on the market could act synogistically with ours.”

Trials are also underway to determine how T-VEC might do with other cancers. In the meantime, other researchers will continue to crack the codes of other viruses to make them do our bidding.