Herpes Vaccine Candidates

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Friday, October 15, 2021 - 06:15

Can mRNA Vaccines Defeat Herpes?

Don Hackett — Thu, 29 Apr 2021 19:41:11 +0000

Reviewer:

REcording of Harvey's Meeting

A research team at the University of Pennsylvania (UPenn) has been working on preventing and treating genital herpes (HSV-2) for years and recently found success with an mRNA vaccine approach, even before the COVID-19 pandemic.

The goals of a HSV-2 vaccine are to keep the herpes virus dormant. Or if the virus escapes, prevent it from causing symptoms.

Professor Harvey M. Friedman demonstrated success in animal models in July 2020. This study found not only targeting entry molecules, but also targeting the HS-2 ability to evade the immune system.

And, in collaboration with UPenn professor Drew Weissman, M.D., Ph.D., they are producing an mRNA vaccine. Dr. Weissman is an inventor of the COVID-19 mRNA vaccine approach, recently authorized by the U.S. Centers for Disease Control and Prevention (CDC).

The CDC stated during March 2021, mRNA vaccines teach human cells how to make a protein, or even just a piece of a protein, that triggers an immune response inside our bodies.

The benefit of mRNA vaccines, like all vaccines, is those vaccinated gain protection without ever having to risk the severe consequences of getting sick.

In the past, HSV-2 prevention vaccine clinical studies (Chiron 1999, GSK 2002 & 2012) targeted the molecules that the herpes virus needed to enter cells using a protein vaccine. These showed some benefits but did not meet the trial designs’ primary endpoints of preventing genital disease.

In the herpes animal models of mice and guinea pigs, the antibody response was found three times greater, and the CD4 T-cells were ten times better with the mRNA vaccine than the protein vaccine.

This superior molecular response was consistent with symptom reduction - the mRNA vaccine was perfect in preventing genital disease (100%) and significantly reduced recurrent disease (98%).

The duration and strength of the mRNA vaccine candidate protection were also better compared to a protein vaccine.

Studying guinea pigs over eight months, equivalent to 20 years in humans, the antibody response was 10x better with the mRNA vaccine after their vaccination. The mRNA vaccine reduced days with the genital disease to <1%, compared to 20% with the protein vaccine.

The risk of transmission (measured by days) was 2% with the protein vaccine, compared to 0% with the mRNA vaccine.

Dr. Friedman says a therapeutic vaccine needs to stimulate CD8 T-cells as opposed to CD4 T-cells.

On February 12, 2021, Dr. Friedman offered his insights in a free video hosted by Blue Jeans.

Dr. Friedman is ready to launch a herpes mRNA vaccine phase 1 human trial in early 2022. He and UPenn have established a donation page to accelerate the funding for this research. The donation page can be found on this webpage.

PrecisionVaccinations publishes research-based vaccine news.

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UPenn HSV2 vaccine candidate embraces mRNA technology

References:

Harvey M. Friedman, MD

An HSV-2 nucleoside-modified mRNA genital herpes vaccine containing glycoproteins gC, gD, and gE protects mice against HSV-1 gen

New Penn-Developed Vaccine Prevents Herpes in Mice, Guinea Pigs

Vaccines to prevent genital herpes

CDC: mRNA Vaccines

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Thursday, April 29, 2021 - 13:15

What Causes Sudden Herpes Virus Outbreaks?

Don Hackett — Sat, 13 Feb 2021 16:34:33 +0000

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Neuronal hyperexcitability is a DLK-dependent trigger of herpes simplex virus reactivation that can be induced by IL-1

University of Virginia (UVA) researchers have offered new insights on what causes herpes simplex virus (HSV-1) to flare up, explaining how stress, illness, and even sunburn can trigger unwanted outbreaks.

These researchers identified HSV-1 co-opts an innate immune pathway resulting from IL-1 stimulation of neurons to induce reactivation.

The discovery could lead to new ways to prevent cold sores and recurrent herpes-related eye disease from reoccurring, the researchers reported on February 11, 2021

“Herpes simplex recurrence has long been associated with stress, fever, and sunburn,” said researcher Anna R. Cliffe, of UVA’s Department of Microbiology, Immunology, and Cancer Biology, in a press statement.

Once infected with HSV, the virus never really goes away. Instead, it lurks inside neurons, waiting for the right moment to strike again, a process known as reactivation, added Dr. Cliffe.

Cliffe and her collaborators found that when neurons harboring the virus were exposed to stimuli that induce “neuronal hyperexcitation,” the virus senses this particular change and seizes its opportunity to reactivate.

In response to prolonged periods of inflammation or stress, the immune system releases a particular cytokine, Interleukin 1 beta.

This cytokine is also present in epithelial cells in the skin and eye and is released when these cells are damaged by ultraviolet light.

Interleukin 1 beta then increases the excitability in the affected neurons, setting the HSV stage to flare up, the UVA researchers discovered.

“It is remarkable that the virus has hijacked this pathway that is part of our body’s immune response,” Cliffe said. “It highlights how some viruses have evolved to take advantage of what should be part of our infection-fighting machinery.”

These UVA researchers demonstrate HSV-1 reactivation from latently infected mouse neurons induced by forskolin requires neuronal excitation. Stimuli that directly cause neurons to become hyperexcitable also induced HSV-1 reactivation.

Forskolin-induced reactivation was dependent on the neuronal pathway of DLK/JNK activation. It included an initial wave of viral gene expression independent of histone demethylase activity and linked to histone phosphorylation.

IL-1β is released under conditions of stress, fever, and UV exposure of the epidermis, all known triggers of clinical HSV reactivation.

They found that IL-1β induced histone phosphorylation and increased sympathetic neurons’ excitation. Importantly, IL-1β triggered HSV-1 reactivation, which was dependent on DLK and neuronal excitability.

The scientists say that more research is needed to fully understand the potential factors which play into herpes simplex disease. It may vary depending on the virus strain or the type of neuron infected.

“A better understanding of what causes HSV to reactivate in response to a stimulus is needed to develop novel therapeutics,” Cliffe said. “Ultimately, what we hope to do is target the latent virus itself and make it unresponsive to stimuli such as Interleukin 1 beta.”

Herpes simplex virus-1 (HSV-1) is one of the most common human pathogens present in approximately 40–90% of the population worldwide. Cold sores, also known as fever blisters, are among the most common symptoms of HSV reactivation.

HSV-1 is mainly transmitted by oral-to-oral contact to cause oral herpes and cause genital herpes. Herpes infections are most contagious when symptoms are present but can still be transmitted to others in the absence of symptoms, says the World Health Organization.

However, recurrent reactivation can lead to herpes keratitis - a severe eye disease which, if left untreated, can result in blindness. In extreme cases the virus can cause encephalitis.

The development of protective HSV vaccines has been an ongoing challenge for decades. Many vaccine candidates are under development, including DNA, modified mRNA, protein subunit, killed virus, and attenuated live virus vaccines.

Early-stage clinical trials to test therapeutic (intended to reduce viral shedding in people who are already infected with HSV) and preventive (designed to prevent infection) vaccine candidates are ongoing.

The researchers have published their findings in the scientific journal eLife. The research team consisted of Sean R. Cuddy, Austin R. Schinlever, Sara Dochnal, Philip V. Seegren, Jon Suzich, Parijat Kundu, Taylor K. Downs, Mina Farah, Bimal N. Desai, Chris Boutell, and Cliffe.

The work was supported by the National Institutes of Health’s National Institute of Neurological Disorder and Stroke, grant R01NS105630; the National Institute of Allergy and Infectious Diseases, and others.

No industry conflicts of interest were disclosed.

PrecisionVaccinations publishes research-based herpes virus vaccine news.

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Neuronal hyperexcitability is a DLK-dependent trigger of HSV-1 reactivation

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WHO: Herpes simplex virus

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Herpes Vaccine Candidates Have Alternative Approaches

Don Hackett — Sun, 08 Nov 2020 19:22:57 +0000

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The R2 non-neuroinvasive HSV-1 vaccine affords protection from genital HSV-2 infections in a guinea pig model

The worldwide need for an effective herpes simplex virus (HSV) vaccine remains a priority because it is a common infection that causes physical and economic disadvantages.

A new study published by Nature on November 6, 2020, reported the recent ‘failure of the subunit gD2 vaccine in a clinical trial demonstrated that new approaches to HSV vaccines are needed, especially those that present multiple HSV antigens.’

‘R2 is an attractive candidate because it is specifically ablated for retrograde axonal transport and therefore fails to invade the peripheral and central nervous systems, as initially demonstrated in mice and validated here in guinea pigs.’

‘The potential utility of a non-neuroinvasive HSV variant as a vaccine is highly regarded. However, early mutant viruses that were attenuated for neurotropism generally had broader replication defects in vivo that limited antigen presentation.’

Nebraska’s Gary Pickard and Patricia Sollars, alongside Northwestern’s Gregory Smith and Tufts University’s Ekaterina Heldwein, have spent years studying how to prevent HSV from reaching the safety of the nervous system, stated a University of Nebraska press release issued on November 6, 2020.

“You can keep the virus from getting into the nervous system,” said Pickard, professor of veterinary medicine and biomedical sciences at Nebraska. “But when you knock down the virus so much that it doesn’t replicate well, you are not rewarded with a robust immune response that can protect you from future exposures.”

Excerpts from this new study are inserted below:

The R2 design offers another solution to the challenge of producing a virus that replicates in the periphery inducing a strong immune response without seeding the nervous system and establishing a latent infection.

Instead of adjusting tissue tropism, R2 selectively eliminates retrograde axonal transport, which is fundamental to neuroinvasion. The design leaves all viral antigens intact for enhanced vaccine efficacy.

Thus, selective elimination of retrograde delivery to the nervous system is an attractive approach for the development of HSV vaccines, because it decreases concerns that a live-attenuated HSV vaccine could become latent, possibly revert or recombine, or subsequently cause complications if the immune system becomes compromised or distressed.

Similarly, the concerns that a persistent HSV vaccine virus could contribute to neurodegenerative diseases, such as Alzheimer’s disease, are eliminated.

The R2 vaccine encodes a mutated UL37 gene which contains three evolutionarily conserved surface-exposed regions: R1, R2, and R3.

Mutation of R2 produces viruses that propagate normally at peripheral sites of inoculation but fail to invade the nervous system by retrograde axonal transport, cannot establish a latent infection, and are avirulent.

The ability to selectively eliminate the neuroinvasive property of these viruses, without otherwise impairing their replication and thus the induction of immunity, provides an intriguing immunization paradigm.

The initial use of an HSV-1 R2 vaccine reflects the importance of HSV-1 in genital HSV infections and the importance of cross-protection, as both HSV-1 and HSV-2 are important human pathogens.

Evidence for cross-protection can be found in many animal experiments. In the recent clinical trial, a gD2 vaccine was more protective against HSV-1 than HSV-2.

Nevertheless, an R2 derivative of HSV-2 will be produced to determine if vaccine efficacy is further enhanced.

In the experiments reported here, we first evaluated the attenuation of the R2 vaccine following vaginal inoculation of guinea pigs, reasoning that this is a sensitive and well-described model of HSV pathogenesis. Interestingly, although the parent F strain was attenuated relative to HSV-1 strain 17syn+ in guinea pigs as we have noted previously, the R2 derivative was further attenuated, non-neuroinvasive, and avirulent.

Thus, R2 was also not detected in the DRG either early during infection or at day 28, times when the parent F strain and wild-type strain 17 syn+ were readily detected.

We next evaluated the protection afforded by the R2 vaccine against vaginal HSV-2 challenge.

R2 was administered by three routes (IM, ID, and IVag) and its efficacy was compared to a gD2+MPL/Alum vaccine, similar to the one used in the clinical trial. This comparison was intended to determine if R2 was at least as effective as the subunit vaccine and if R2 was more effective in the important outcomes regarding recurrent disease and recurrent virus shedding.

Therefore, we used the guinea pig genital model because it uniquely allows for the evaluation of these critical endpoints. The advantages of this model are more fully discussed in a recent review.

Protection was detected by R2 immunization using all 3 routes of vaccination but the ID route was consistently the most effective. Importantly, ID administration of the R2 vaccine-induced higher levels of neutralizing antibodies and provided greater protection than the gD2 subunit vaccine by several parameters.

Perhaps, this was due to the improved neutralizing antibody response and/or the ability of live-attenuated virus vaccines to induce T cell-mediated immunity that exceeds that of subunit vaccines.

In the experiments reported here, R2 vaccination by the ID route protected the most animals from acute disease and had the largest decrease in acute virus replication. R2 vaccination also decreased latent virus detection in the DRG as well as recurrent disease and recurrent shedding.

In comparison, the gD2 MPL/alum vaccine did not significantly decrease the number of animals with acute disease, acute vaginal virus titers, or recurrent vaginal virus shedding. Only further clinical evaluations of vaccines that have been evaluated in this guinea pig model will allow a better understanding of predictability.

There are several anomalies that should be pointed out in our data. The most important is the discrepancy between the number of animals with latent virus detected in the DRG and recurrent shedding. While we cannot currently reconcile these findings, one possible explanation is that gD2 MPL/Alum failed to protect against invasion and reactivation of HSV-2 from another latent site, perhaps autonomic neurons.

In summary, the live R2 HSV-1 vaccine is significantly attenuated in the guinea pig vaginal model and most importantly does not infect the nervous system within the limits of detection. R2 vaccination, especially by the ID route, provided protection against acute disease, recurrent disease, and recurrent virus shedding that was equal or superior to the gD2+MPL/Alum vaccine.

Given the encouraging findings with R2, a more detailed analysis of the correlates of protection is warranted and will be examined as part of future studies.

We consider these results highly encouraging, especially considering R2 is an HSV-1 virus and was evaluated for cross-protection against HSV-2 challenge.

Because no HSV vaccines have yet proven effective clinically, it is not clear what endpoints of the guinea pig vaginal model will predict protection in human evaluations, concluded these researchers.

These researchers did not disclose industry conflicts of interest.

PrecisionVaccinations publishes research-based herpes vaccine development news.

Sub Title:

Non-neuroinvasive herpes simplex virus variant could be a highly regarded vaccine candidate

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A new era in cytomegalovirus vaccinology: considerations for rational design of next-generation vaccines to prevent congenital c

Vaccine shows promise against herpes virus

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Curing Herpes Comes Into Focus

Don Hackett — Wed, 19 Aug 2020 11:37:08 +0000

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Gene editing and elimination of latent herpes simplex virus in vivo

Fred Hutchinson Cancer Research Center researchers have been exploring the idea that lifelong infections with herpes viruses might be cured by using the DNA-cutting tools of gene therapy.

The initial research showed these techniques could knock out small quantities of latent virus, and the work of improving the study's results fell to virologists Dr. Keith Jerome Jerome and Dr. Martine Aubert.

This team has just published a paper in Nature Communications on August 18, 2020, showing that, through a series of incremental improvements on their original method, they had destroyed up to 95 percent of herpes virus lurking in certain nerve clusters of mice. Much of the team’s meticulous work of the past 5-years has involved finding better ways to target infected clusters of nerve cells and to thwart the virus’s ability to quickly repair the cuts to its genes.

“This is the first time that anybody has been able to go in and actually eliminate most herpes in a body,” said Dr. Jerome, who is also spearheading research at Fred Hutchinson.

“It is a completely different approach to herpes therapy than anybody’s ever had before. I hope that this study changes the dialogue around herpes research and opens up the idea that we can start thinking about a cure, rather than just control of the virus,’ commented Dr. Jerome in a press statement.

The hidden herpes viruses are disabled by an injection that tracks down infected nerve cells and induces them to make special gene-cutting enzymes, which work like molecular scissors, to slash viral genes in specific places.

Whereas most research on herpes has focused on suppressing the recurrence of painful symptoms, the Fred Hutch gene therapy work addresses the root cause of reactivation: the presence of the latent virus in infected nerve cells.

It will still take a long time before these mice experiments lead to human clinical trials to cure herpes. Dr. Jerome estimates that will be at least three years away.

The Jerome Lab’s herpes research thus far involves only HSV-1, but the scientists are now working on ways to extend their success to HSV-2. The first step will be to repeat their experiments using HSV-2 in guinea pigs, which, unlike mice, experience natural reactivations of herpes virus infections, just as humans do.

The advances in herpes cure research over the past five years are largely due to a series of improvements in the gene-editing tools. First, the researchers added combinations of different gene-cutting enzymes. The more cuts these molecular scissors make, the harder it is for the virus to recover.

Second, they chose different strains of harmless carrier viruses that do a better job of transporting those cutting tools to the places in the body where infected nerve cells are clustered.

“It’s been three or four years of work, but I think what we describe in the paper is a really big step,” said Dr. Aubert. “It gets us closer to really considering this as a curative approach. It gives us the green light.”

Since the earliest days of the experiments, the Jerome team learned to rely on a cutting enzyme called a “meganuclease” that can zero in on a segment of herpes DNA and cut both strands of the double helix. Despite the “mega” in its name, these scissors are extraordinarily small — about half the size of an antibody, those tiny, Y-shaped proteins our immune system uses to swarm over and disable viruses and bacteria.

The team attained its first promising results years ago using a single type of meganuclease that proved effective in cutting the herpes virus DNA, but the results were short-lived. The virus could rely on the infected cells’ own DNA-repair programs — which don’t distinguish between viral genes from their own — to fix the break most of the time.

But over time, the researchers found that they could eliminate up to 90% of the latent virus by using a mix of two or three different meganucleases. It is simply harder to repair two breaks than one. With more tinkering, the results continued to improve.

The researchers also refined their methods of transporting molecular scissors to targeted nerve cells. From the beginning, Jerome and his team have relied on a harmless, hollowed-out virus that is drawn to the surface proteins of nerve cells.

Called an adeno-associated virus vector, or AAV, it is the little workhorse of gene therapy. In this case, it is used to ferry to the infected nerve cells' genetic instructions that cause them to make those meganucleases.

“We inject the AAV vector, and it finds its way,” Aubert said.

Latent herpes viruses lurk in clusters of nerve cells called ganglia, and researchers have found that some ganglia are harder to reach than others. Over the years, they discovered that some AAV strains are better suited than others to find specific types of nerve clusters, and this has helped them fine-tune the selection of these delivery viruses to match infected cells in different places.

In their mouse experiments, the team continued to improve their results, nudging them up to a 95% reduction in herpesvirus infection in one prominent nerve cluster using a selection of two different meganucleases carried by three different flavors of AAVs. By selecting vectors that are primed for harder-to-reach nerve clusters, the group expects to continue improving their ability to eradicate the virus.

As the Jerome Lab prepares to see if its gene therapy can block genital herpes, they are also reshuffling their selection of vector viruses and meganucleases to target nerve cells infected by HSV-2.

They are collaborating with Dr. Barry Stoddard, a Hutch colleague who specializes in discovering the structure of proteins, to custom-design a set of meganucleases that they hope will work even better than the first.

“The three enzymes they use already work pretty well, but one doesn’t quite work as well as the others,” Dr. Stoddard said. “We’re looking at the structure and determining a few changes to improve performance.”

Stoddard is also tweaking the meganucleases’ structures to make them a better fit against HSV-2.

In their latest paper, the team evaluated the use of a newer and more glamourous gene-cutting tool, CRISPR-Cas9. Somewhat surprisingly, they found that this newfangled precision cutting tool did not perform as well as their meganucleases.

One possible reason: CRISPR is a much larger molecule, and the comparatively smaller meganucleases are easier to package and deliver to nerve cells.

Stoddard said that meganucleases can also more accurately zero in on their target genes than CRISPR, which is known for its “off-target” effects — cutting the wrong gene. The advantage of CRISPR is that it can be designed quickly, while meganucleases are laborious to make.

”It can take a day to make a new CRISPR. It takes about three months to make a meganuclease," Stoddard said.

Experience has shown, however, that the Jerome Lab is endowed with patience. Their 10-year trek has proven the potential of gene therapy for erasing herpes, yet the road ahead will undoubtedly require deep reserves of patience and persistence.

Although the antiviral drug acyclovir can knock down an outbreak of HSV-2, the virus lingers for a lifetime within infected nerve cells and may reactivate, causing recurrent bouts of painful sores, on average, up to 7 times per year.

The prevalence of this chronic disease increases with age. Less than 1 percent of teens in the USA are infected, but that increases to 21 percent of Americans in their 40s, according to the Centers for Disease Control and Prevention.

This new research was supported by the Caladan Foundation and the National Institutes of Health. Meganucleases used in the experiments described in the Nature Communications paper were supplied by Paris-based Cellectis SA. Scientists at Fred Hutch played a role in developing these discoveries, and Fred Hutch and certain of its scientists may benefit financially from this work in the future.

Herpes vaccine candidates are in various stages of clinical research and are listed on this PrecisionVaccinations webpage.

PrecisionVaccinations publishes research-based herpes vaccine news.

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Herpes virus targeted by gene cutting enzymes

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Oral Herpes Rates Declining in Europe

Don Hackett — Fri, 24 Jul 2020 13:55:28 +0000

Reviewer:

Herpes simplex virus type 1 in Europe: systematic review, meta-analyses and meta-regressions

Over 65 percent of young people have their first sexual activity unexposed to herpes, but risk catching it in adulthood, stated a new study.

This research found fewer people are being exposed to herpes simplex type 1 (HSV-1), also known as oral herpes in their youth.

HSV-1 is mainly transmitted by oral-to-oral contact during childhood, causing oral herpes, but it can also cause genital herpes. The other form of the virus (HSV-2) is sexually transmitted and causes genital herpes.

Furthermore, this research published in BMJ Global Health on July 16, 2020, suggests the prevalence of oral herpes amongst Europeans is falling by 1 percent per year.

This study’s findings indicate the prevalence of the herpes virus, which often manifests itself with cold sores, appears to be declining in younger people.

Previous research data focused on North America and Europe has suggested that there is a decrease in the acquisition of HSV-1 in childhood, a decline in its population prevalence in youth, and an increase in genital herpes cases that are caused by HSV-1.

For this study, a team of researchers from Weill Cornell Medicine-Qatar of Cornell University set out to examine the epidemiology of HSV-1 in Europe.

They systematically reviewed HSV-1 related publications, conducted various meta-analyses, assessed pooled prevalence rates in populations, and estimated pooled proportions of HSV-1 viral detection in clinically diagnosed genital ulcer disease and in genital herpes.

Their analysis gathered information from 142 suitable previous publications. From these publications, they extracted 179 overall population prevalence measures, four overall proportions of HSV-1 in genital ulcer disease, and 64 overall proportions of HSV-1 in genital herpes.

The results showed that more than two-thirds (67.4%) of the population in Europe tested positive for HSV-1, which is far lower than the historical level of universal infection in childhood in other parts of the world, such as Africa.

Around 32.5% of children and 74.4% of adults were infected in Europe.

Prevalence in the population increased steadily with age, being lowest in those aged below 20 years and highest in those aged over 50 years.

The researchers speculated that reasons for falling prevalence rates of HSV-1 could include a general decrease in both family size and school crowding, as well as improved hygiene and living conditions.

The results also showed that half of the first-episode genital herpes cases in Europe were already due to HSV-1, as opposed to HSV-2 infection.

Both forms of the herpes virus are lifelong and the World Health Organization (WHO) estimates there are 3.7 billion people under age 50 (67%) who have HSV-1 infection globally and 491 million people aged 15-49 (13%) worldwide with HSV-2 infection.

The study authors acknowledged that their systematic review had some limitations, primarily the unavailability of data for 25 of 53 European countries, and had comparatively less data for genital ulcer disease and genital herpes than population prevalence.

Nevertheless, these limitations did not appear to have posed a barrier to the interpretation of the results of the study, they said.

These researchers stated: “HSV-1 transition in Europe is leading to more heterogeneous and variable transmission by age and geography, and an increasing role for HSV-1 in genital herpes as a sexually transmitted disease.”

“The findings highlight the importance of disease surveillance and monitoring of HSV-1 seroprevalence and genital herpes etiology, and strengthen the case for an HSV-1 vaccine to limit transmission.”

Clinical researchers have been working on developing herpes vaccines in clinical trials focused on both therapeutic and preventive vaccine candidates, which are listed on this webpage.

Herpes vaccine news is published by Precision Vaccinations.

Sub Title:

European children HSV1 infection rate exceeds 32 percent

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Herpes Impacts Women’s Reproductive Health

Don Hackett — Sat, 02 May 2020 16:23:23 +0000

Reviewer:

WHO: Herpes simplex virus: global infection prevalence and incidence estimates, 2016

Kelley Lu, PharmD

A new study estimates about half a billion people are living with genital herpes, and several billion have oral herpes infections around the world.

Herpes simplex virus (HSV) infections are lifelong and characterized by periodic reactivations. Symptomatic and asymptomatic viral shedding is common for both types of herpes.

Thus, infected individuals can be asymptomatic, yet infectious, allowing these viruses to be transmitted unknowingly. This attribute contributes to the large global prevalence of herpes infections.

And this study reports HSV type 2 (HSV-2) infections disproportionately affected women.

This insight means that HSV has a substantial effect on the sexual and reproductive health of millions of people worldwide.

Published by the World Health Organization (WHO) on May 1, 2020, these European researchers highlight the need to improve the awareness of products to prevent and treat herpes cases.

This study estimates around 491 million people currently living with HSV-2 infection, 3.5 billion with oral HSV type 1 (HSV-1) infection, and 122 million –192 million with genital HSV-1, in those up to 49 years of age.

Herpes Overview

HSV type 1 (HSV01) is primarily transmitted by oral-to-oral contact and cause orolabial herpes, which is commonly known as cold sores.

Type 1 virus also causes rarer conditions, such as keratitis and other ocular sequelae, and encephalitis.

HSV-1 genital infection from oral-to-genital contact is becoming increasingly common, although reactivations are less frequent than for HSV-2.

HSV-2 is almost entirely sexually transmitted, causing genital herpes.

Genital HSV infection may be unrecognized or result in painful genital ulcer disease in a proportion of those infected.

Neonates can acquire HSV infection from genitally infected mothers during birth and from oral contact with caregivers postnatally.

Neonatal infection, although rare, has a high fatality and disability rate in surviving infants. There is no cure for herpes today, says the WHO.

Herpes treatments

Most herpes infections are self-limited and treatment is not always indicated or necessary.

The current WHO guidelines provide 6 treatment recommendations for genital HSV infections. A summary of recommendations for genital HSV infection treatments can be found here.

There are intravenous, oral, and topical antiviral herpes medications, such as acyclovir, famciclovir, and valacyclovir, that can help to reduce the severity and frequency of symptoms.

Herpes Vaccine Candidates

As of May 2, 2020, the U.S. Food and Drug Administration has not approved any herpes preventive vaccine. However, after many years of research, various herpes vaccine candidates are making progress to FDA approval.

These herpes vaccine candidates include, but are not limited to the following list:

HSV529 is a vaccine candidate that is classified as a replication-defective virus, where the virus possesses all the components of the wild-type HSV virus with the exception of two proteins UL5 and UL29 that are involved in viral DNA replication.
EXD-12 vaccine candidate is currently in preclinical testing for safety and efficacy as both a prophylactic and therapeutic vaccine for both Herpes Simplex Virus-1, HSV-1, and Herpes Simplex Virus-2, HSV-2.
GSK’s HSV Vaccine or SB208141 is in a double-blind, randomized, controlled phase 3 clinical study to assess the prophylactic efficacy and safety of gD-Alum/MPL vaccine in the prevention of genital herpes disease in young women who are herpes simplex virus (HSV)-1 and -2 seronegative.

This new study was funded by the WHO Department of Reproductive Health and Research, via support from the United States NIH (U01 AI108543).

The researchers reported these competing interests: KJL reports grants from WHO during the conduct of the study and outside the submitted work. KJL and KMET report a grant from GSK outside the submitted work. NJW reports grants from the National Institute for Health Research during the conduct of the study and grants from Pfizer Ltd outside the submitted work. SLG reports grants from NIH during the conduct of the study.

Herpes vaccine development news published by Precision Vaccinations.

Sub Title:

Genital or Oral Herpes cases exceed 1 billion

References:

WHO: Billions worldwide living with herpes