Herpes linked to Alzheimer's: Antivirals may help

A new commentary by scientists at the Universities of Manchester and Edinburgh on a study by Taiwanese epidemiologists supports the viability of a potential way to reduce the risk of Alzheimer's disease.

When the Taiwanese authors looked at subjects who suffered severe herpes infection and who were treated aggressively with antiviral drugs, the relative risk of dementia was reduced by a factor of 10.

Manchester's Professor Ruth Itzhaki and Edinburgh's Professor Richard Lathe say the paper, by Tzeng et al. and published in Neurotherapeutics in February 2018, also shows that herpes simplex virus type 1 (HSV1) leads to an increased risk of developing the disease.

"This article and two others by different research groups in Taiwan provide the first population evidence for a causal link between herpes virus infection and Alzheimer's disease, a hugely important finding," said Professor Itzhaki.

They publish a commentary in the Journal of Alzheimer's Disease on the three articles, arguing that they provide the strongest evidence yet for a causal link between herpes infection and Alzheimer's disease, backing 30 years of research by Professor Itzhaki.

Professor Itzhaki said: "I believe we are the first to realise the implications of these striking data on this devastating condition which principally affects the elderly. No effective treatments are yet available.

"Almost 30 million people worldwide suffer from it and sadly, this figure will rise as longevity increases.

"But we believe that these safe and easily available antivirals may have a strong part to play in combating the disease in these patients.

"It also raises the future possibility of preventing the disease by vaccination against the virus in infancy.

"Successful treatment by a specific drug, or successful vaccination against the putative microbe, are the only ways to prove that a microbe is the cause of a non- infectious human disease."

Most Alzheimer's disease researchers investigate its main characteristics -- amyloid plaques and neurofibrillary tangles; however, despite the vast amount of research, the causes of their formation are unknown.

HSV1 infects most humans in youth or later and remains lifelong in the body in dormant form within the peripheral nervous system.

From time to time the virus becomes activated and, in some people, it then causes visible damage in the form of cold sores.

The Taiwanese study identified 8,362 subjects aged 50 or more during the period January to December 2000 who were newly diagnosed with severe HSV infection.

The study group was compared to a control group of 25,086 people with no evidence of HSV infection.

The authors then monitored the development of dementia in these individuals over a follow-up period of 10 years between 2001 and 2010.

The risk of developing dementia in the HSV group was increased by a factor of 2.542. But, when the authors compared those among the HSV cohort who were treated with antiviral therapy versus those who did not receive it, there was a dramatic tenfold reduction in the later incidence of dementia over 10 years.

Professor Richard Lathe added: "Not only is the magnitude of the antiviral effect remarkable, but also the fact that -- despite the relatively brief duration and the timing of treatment -- in most patients severely affected by HSV1 it appeared to prevent the long-term damage in brain that results in Alzheimer's.

Professor Itzhaki said: "It was as long ago as 1991 when we discovered that, in many elderly people infected with HSV1, the virus is present also in the brain, and then in 1997 that it confers a strong risk of Alzheimer's disease in the brain of people who have a specific genetic factor.

"In 2009, we went on to show that HSV DNA is inside amyloid plaques in Alzheimer's patients' brains.

"We suggested that the virus in brain is reactivated by certain events such as stress, immunosuppression, and infection/inflammation elsewhere.

"So we believe the cycle of HSV1 reactivation in the brain eventually causes Alzheimer's in at least some patients."

Source: https://www.sciencedaily.com/releases/2018/07/180712100515.htm

Sexually Transmitted Diseases Co-Infections

Chlamydia & Gonorrhoea Co-infection

Co-infection is the outcome of contracting a second STD while already actively infected with an STD. The most common use of the term co-infection is in reference to Gonorrhoea and chlamydia, which often occur together. The two infections are discovered together so often that it is actually recommended to get tested for both at the same time. Data released by the Virgina Department of Health supports the estimate that between 40 and 50 percent of all young adults infected with Gonorrhoea also have a chlamydia infection, with women more likely to have a co-infection than men. The risk of testing positive for both chlamydia and Gonorrhoea also increased when the use of drugs or alcohol was reported. Both chlamydia, which is caused by the Chlamydia trachomatis bacteria, and Gonorrhoea, caused by Neisseria gonorrhoeae bacteria, can be treated with antibiotics. If the infection is caught early enough, sometimes only a single dose of antibiotics is needed.

HIV Co-infections

Human immunodeficiency virus (HIV) is an incurable viral infection that attacks the immune system, destroying the infected person’s ability to fight off infection and disease. People living with HIV run a much higher risk of suffering from an STD co-infection than the HIV-negative community. The amount of HIV found in the genital secretions, known as the viral load, is much higher in people with an active STD infection. If HIV is left untreated, it progresses into the terminal late-stage known as Acquired Immune Deficiency Syndrome (AIDS). By the time HIV becomes AIDS, the patient has lost so much immune capability that they are extremely susceptible to infections, including STDs. Approximately 25% of people with HIV will also suffer from tuberculosis, which is the second highest cause of death for people living with HIV/AIDS. HIV co-infection is a serious and life-threatening condition that can be prevented.

HIV and Syphilis

HIV and syphilis have a long history of co-infection. According to a report conducted by the state of Virginia, approximately one-third of all new cases of syphilis diagnosed in Virginia were in individuals who had previously been diagnosed with HIV. The rate of syphilis infection in the HIV-positive community is 118 times higher than the general population. Receptive anal sex is considered a high risk behavior for contracting STDs because of the ease of damaging anal tissue, which allows a path for STDs to move between bodies via sexual fluids, such as semen. For this reason, men who have sex with men are the most affected by HIV and syphilis co-infection, with the state of Virginia reporting that 99.5 percent of all HIV/syphilis co-infections were among males, with 90 percent of those males engaging in sex with another man.

HIV and Gonorrhoea

While gonorrhoea, known as “the clap,” and chlamydia are the most closely linked of all co-infections, gonorrhoea also has a close tie to HIV. According to data released by the Washington State Department of Health, approximately 6 percent of all people diagnosed with Gonorrhoea were already living with HIV. Developing an immunity to HIV medications, as well as the chance of contracting an antibiotic-resistant strain of Gonorrhoea make this combination of infections particularly serious.

HIV and Hepatitis C

The World Health Organization states that 170 million people have been diagnosed with hepatitis C in the past century, making it an epidemic on a larger scale than even HIV, which has resulted in about 79 million diagnoses since the start of the HIV Epidemic. Hepatitis C is an incurable infection that has many life-threatening side effects, such as liver failure, cirrhosis, and cancer. Hepatitis also makes it more difficult for the immune system to properly fight off infection, making it easier to also become infected with HIV. Antiviral medications are prescribed to treat hepatitis C, as well as HIV. The biggest factor in contracting HIV when an active hepatitis C infection is present is the patient’s behavior, which includes intravenous drug use or unprotected sex in many cases. Being diagnosed with hepatitis C while living with HIV is one of the criteria for receiving an AIDS diagnosis. About 25% of HIV-positive Americans also have hepatitis C.

Submit your abstracts for the STD 2018 conference under the track - Co-Infections of STDs. To know more, visit: https://std-hiv-aids.cmesociety.com/call-for-abstracts/co-infection-of-stds

Source: https://www.stdcheck.com/blog/hiv-std-coinfection/

New anti-viral nanoparticles that destroy broad spectrum of viruses including ‘HIV’

Viral infections kill millions of people worldwide every year, but currently available antiviral drugs are limited in that they mostly act against one or a small handful of related viruses. A few broad-spectrum drugs that prevent viral entry into healthy cells exist, but they usually need to be taken continuously to prevent infection, and resistance through viral mutation is a serious risk.

Now, an international group of researchers including UIC professor of chemistry Petr Kral, have designed new anti-viral nanoparticles that bind to a range of viruses, including herpes simplex virus, human papillomavirus, respiratory syncytial virus and Dengue and Lentiviruses. Unlike other broad-spectrum antivirals, which simply prevent viruses from infecting cells, the new nanoparticles destroy viruses.

The new nanoparticles mimic a cell surface protein called heparin sulfate proteoglycan (HSPG). A significant portion of viruses, including HIV, enter and infect healthy cells by first binding to HSPGs on the cell surface. Existing drugs that mimic HSPG bind to the virus and prevent it from binding to cells, but the strength of the bond is relatively weak. These drugs also can’t destroy viruses, and the viruses can become reactivated when the drug concentration is decreased.

Kral and his colleagues, including Lela Vukovic, assistant professor of chemistry at the University of Texas at El Paso and an author on the paper, sought to design a new anti-viral nanoparticle based on HSPG, but one that would bind more tightly to viral particles and destroy them at the same time.

“We knew the general composition of the HSPG-binding viral domains the nanoparticles should bind to, and the structures of the nanoparticles, but we did not understand why different nanoparticles behave so differently in terms of both binding strength and preventing viral entry into cells,” said Kral.

Through elaborate simulations, Kral and colleagues helped solve these issues and guided the experimentalists in tweaking the nanoparticle design so that they worked better.

The researchers used advanced computational modeling techniques to generate precise structures of various target viruses and nanoparticles down to the location of each atom. A deep understanding of the interactions between individual groups of atoms within the viruses and nanoparticles allowed the researchers to estimate the strength and permanence of potential bonds that could form between the two entities, and helped them to predict how the bond could change over time and eventually destroy the virus.

The team’s final “draft” of the anti-viral nanoparticle could bind irreversibly to a range of viruses, and caused lethal deformations to the viruses, but had no effect on healthy tissues or cells. In vitro experiments with the nanoparticles showed that they bound irreversibly to the herpes simplex virus, human papillomavirus, syncytial virus, Dengue virus and Lentivirus.

“We were able to provide the data needed to the design team so that they could develop a prototype of what we hope will be a very effective and safe broad-spectrum anti-viral that can be used to save lives,” said Kral.

Source: https://www.sciencedaily.com/releases/2017/12/171218154928.htm

Early ART treatment tied to HIV remission

The research on early antiretroviral therapy has led to the fact that treatment of the virus during infancy may suppress HIV to undetectable levels which could reduce the need for life-long drug therapy. In the study, before treatment, the child’s levels of HIV in the blood, or viral load, were very high. At around 9 weeks of age, the child started ART, which suppressed the virus to undetectable levels. The child’s treatment was halted at 40 weeks, and their immune health was monitored during years of follow-up examinations.

Investigators assessed the child’s immune health and the presence of HIV at age 9.5 years. They found a reservoir of virus in a tiny portion of immune cells, but otherwise no evidence of HIV infection was detected and there were no associated symptoms.

While the researchers detected a trace of response by the immune system, they were unable to identify any HIV capable of replicating. It was confirmed that the child does not have genetic characteristics connected with spontaneous HIV control, which suggests that the 40 weeks of ART received during infancy may have played a key role in achieving HIV remission.

Since the initial treatment, the child has maintained undetectable levels of HIV. “To our knowledge, this is the first reported case of sustained control of HIV in a child enrolled in a randomized trial of ART interruption following treatment early in infancy,” says Dr. Avy Violari, head of pediatric research at the Perinatal HIV Research Unit at the University of the Witwatersrand in Johannesburg, South Africa, co-led the study with Mark Cotton, head of the Division of Pediatric Infectious Diseases at Stellenbosch University, also in South Africa.

Source: https://www.medicalnewstoday.com/articles/318636.php