One of the most common viruses throughout the world is the herpes simplex virus; this is categorized into herpes simplex virus type 1 HSV-1 and herpes simplex virus type 2 HSV Globally, nearly 4 billion people under the age of 50 have HSV-1; once a person contracts the virus, they will have it for the duration of their life. Fewer than million people around the world have HSV-2; this variant is a sexually transmitted infection and is not as easily spread from person to person.
HSV-1 is primarily spread through oral contact; when a person has close oral contact with an infected person, whether symptomatic or not, they are at risk of contracting the virus. Oral-to-genital contact can spread HSV-1 to the genital area, as well. HSV-2, however, is almost entirely transmitted during sexual activity involving genital-to-genital or genital-to-anal contact.
Individuals can go for lengthy periods of time without experiencing any symptoms of either variant of the infection; when symptoms do manifest, they often cause blisters or sores at the site of infection, sometimes resulting in severe pain.
As mentioned, there is no cure for an HSV infection; the symptoms of the virus, though, can be addressed through the use of antivirals such as acyclovir and famciclovir. As with many infections, the best treatment is prevention — the regular and correct use of condoms can prevent the spread of HSV-2, and avoiding oral contact — either directly or indirectly, such as through sharing things like lip balm — with individuals displaying active HSV-1 symptoms can stop the spread of this more common form.
This page is designed to show you how to write a research project on the topic you see here. Use our sample or order a custom written research paper from Paper Masters. Related Research Paper Topics. How to Write a Research Paper on Topic This page is designed to show you how to write a research project on the topic you see here.In Maythe World Health Organization WHO estimated that around half a billion people worldwide are living with genital herpes, and several billion have oral herpes.
While there are antiviral medications available to help reduce symptoms, there is no cure. Recently, a paper published in the science journal Nature Communications reported that a team of researchers was able to eliminate over 90 percent of latent herpes simplex virus, which causes oral and genital herpes, in mice.
Terri Wilder: Thanks for being here with me today, Dr. My first question is: Why is herpes simplex virus a public health problem? Keith Jerome: Well, herpes is unique. Once the virus gets into a person, it finds a particular place it likes to essentially fall asleep—we call it latency. But for herpes simplex, it goes to neurons within the body called nerve cells. But every once in a while, the virus can wake up and then travel back out from those nerve cells.
Jerome: Absolutely. Obviously, there are other risk factors for HIV, but on a population-wide basis, particularly in areas where the incidence of HIV infection is very high, along with a high level of herpes simplex virus—for example, in parts of sub-Saharan Africa—we think that almost half of all the HIV cases that exist can actually be traced back to a pre-existing herpes simplex virus infection. So, we could make a tremendous impact there. Acyclovir basically pushes the virus back down into that sleeping phase I mentioned earlier.
There are also a variety of derivatives and second-generation drugs similar to acyclovir that work slightly better or slightly differently. But essentially, they all work by tamping the virus back down. They offer no possibility for cure. Wilder: What proportion of people infected with herpes actually have latent herpes simplex virus?
Jerome: From everything we understand, everyone who becomes infected with herpes simplex establishes latency. Now, that can show itself in very different ways from one individual to the next.
Some people become infected with herpes and never develop any symptoms. Other people might get a lesion or two a year, or a cold sore once a year or so. Those are the people deeply affected by these infections—and, again, we would like to be able to offer a treatment that could actually help eliminate these problems with the virus. Wilder: I read that you started thinking up a possible cure for herpes around 10 years ago.
Jerome: Well, that was when I first became aware of what today has become an area of research that we call gene editing.The Human Herpes Viruses
There are other types, as well. When I first became aware of that, I realized that gene editing proteins have the unique capability of very specifically looking for the DNA—the stuff of life—of, in this case, a virus, and ignore everything else. I realized that gene editing proteins could actually find an infection—whether it was HIV, herpes, or hepatitis B—destroy that DNA, and leave the rest of the body alone. Remember that these sleeping viruses that I mentioned are long-lived forms of DNA within the body.
So if we could destroy the viruses in a very selective manner, we might have a possibility to think about cure. What is it about this virus that makes it so challenging to eliminate? Jerome: Once the virus goes to sleep in the nerve cells, it coils itself up into a little circle. In a lot of ways, that little circle looks a lot like our own DNA. Remember, our cells are all encoded and contain billions of those letters of DNA. Herpes contains aboutarranged in this circle that floats around within the nerve cell.Herpes simplex research includes all medical research that attempts to prevent, treat, or cure herpes, as well as fundamental research about the nature of herpes.
Examples of particular herpes research include drug development, vaccines and genome editing. There are many more members that infect animals other than humans, some of which cause disease in companion animals cats, dogs, horses or have economic impacts in the agriculture industry pigs, cows, sheep.
Various vaccine candidates have been developed, the first ones in the s, but none has been successful to date. Due to the genetic similarity of both herpes simplex virus types HSV-1 and HSV-2the development of a prophylactic-therapeutic vaccine that proves effective against one type of the virus would likely prove effective for the other virus type, or at least provide most of the necessary fundamentals.
As of [update]several vaccine candidates are in different stages of clinical trials. An ideal herpes vaccine should induce immune responses adequate to prevent infection. Short of this ideal, a candidate vaccine might be considered successful if it a mitigates primary clinical episodes, b prevents colonization of the gangliac helps reduce the frequency or severity of recurrences, and d reduces viral shedding in actively infected or asymptomatic individuals.
However, governmental and corporate bodies seem to support the more recent and safer but possibly less effective approaches such as glycoprotein- and DNA-based vaccines. Vaccine-elicited protection against HSV is challenging to achieve due to the ability of herpesviruses to evade many aspects of the mammalian immune response.
As a general principle, the effectiveness of a HSV vaccine design is often inversely proportional to its safety.
What If We Could Finally Cure Herpes? This Scientist Is on the Case
Subunit vaccines, which consist of individual or small groups of viral antigens, remove all risk of complications resulting from the production of vaccine-associated infectious viral particles but are limited in the degree and scope of immunity that can be produced in vaccinated individuals.
Inactivated vaccines, which consist of intact viral particles, dramatically increase the repertoire of viral antigens that engender the immune response but like subunit vaccines are generally constrained to producing humoral immunity.
Like inactivated vaccines, replication-defective vaccines expose the immune system to a diverse swath of HSV antigens but can produce both cellular and humoral immunity because they retain the ability to enter cells by HSV-induced membrane fusion.
However, replication-defective HSV vaccines are challenging to produce at scale and offer limited immunization due to the lack of vaccine amplification. Live-attenuated vaccines are highly efficacious, potentially eliciting both cell-mediated and humoral immunity against structural and non-structural viral proteins, but their ability to replicate can result in vaccine-related illness particularly in immunocompromised individuals.
Whereas subunit vaccines have proven effective against some viruses, immunity produced by subunit HSV vaccines e. Herpevac have failed to protect humans from acquiring genital herpes in several clinical trials.
The challenge of achieving vaccines that are both safe and effective has led to two opposing approaches in HSV vaccine development: increasing the efficacy of subunit vaccines primarily by improving adjuvant formulationsand increasing the safety of live-attenuated vaccines including the development of "non-invasive" vaccines.
The chart below is an attempt to list all known proposed HSV and varicella zoster vaccines and their characteristics. Please update with any missing information on vaccines only.
William Halford . A recent development in live-attenuated HSV vaccine design is the production of replicative vaccines that are ablated for nervous system infection.
Evolutionary origins of human herpes simplex viruses 1 and 2
These vaccines infect the respiratory mucosa where their replication and localized spread provoke a robust immune response. The safety of these vaccines is based on their inability to invade the nervous system and establish life-long latent infections, as opposed to a general attenuation.
Unlike other live-attenuated designs, these vaccines are cleared from the body once the immune response from vaccination has matured. In principle, by avoiding attenuation of HSV replication in the mucosa while removing the capacity to infect the nervous system, non-invasive vaccines have the potential to break the safety-efficacy dilemma by producing the strongest possible immune response while maintaining a high degree of safety. The VC2 non-invasive vaccine was developed by Dr.
Gus Kousoulas at Louisiana State University. VC2 encodes two attenuating mutations that together reduce HSV entry into neurons. The establishment of latency is prevented in animal models such as mice, guinea pig, and rhesus monkeys. The R2 non-invasive vaccine was developed by Drs. R2 vaccines retain native replication in epithelial cells but are incapable of retrograde axonal transport and invasion of the nervous system. This vaccine strategy is noted for its effectiveness against both veterinary and clinical neuroinvasive herpesviruses.
Already proven as safe and effective in rodents and eliciting 10 to times greater protection against genital herpes than a glycoprotein D subunit vaccine, Halford's vaccine was tested outside of the United States, in St.
Kitts in 20 human volunteers. All 20 of the participants self-reported an improvement in symptoms, but only 17 received and completed all three dosages. David M. Knipea Professor at Harvard Medical School has developed dl Herpesviruses have been infecting and codiverging with their vertebrate hosts for hundreds of millions of years.
The primate simplex viruses exemplify this pattern of virus-host codivergence, at a minimum, as far back as the most recent common ancestor of New World monkeys, Old World monkeys, and apes. Human herpes simplex viruses are ubiquitous, with over two-thirds of the human population infected by at least one virus.
Here, we investigated whether the additional human simplex virus is the result of ancient viral lineage duplication or cross-species transmission. We found that standard phylogenetic models of nucleotide substitution are inadequate for distinguishing among these competing hypotheses; the extent of synonymous substitutions causes a substantial underestimation of the lengths of some of the branches in the phylogeny, consistent with observations in other viruses e.
To more accurately estimate ancient viral divergence times, we applied a branch-site random effects likelihood model of molecular evolution that allows the strength of natural selection to vary across both the viral phylogeny and the gene alignment.
This selection-informed model favored a scenario in which HSV-1 is the result of ancient codivergence and HSV-2 arose from a cross-species transmission event from the ancestor of modern chimpanzees to an extinct Homo precursor of modern humans, around 1.
These results provide a new framework for understanding human herpes simplex virus evolution and demonstrate the importance of using selection-informed models of sequence evolution when investigating viral origin hypotheses. Keywords: co-divergence; cross-species transmission; homo; molecular clock; selection; zoonosis. All rights reserved. For permissions, please e-mail: journals. Abstract Herpesviruses have been infecting and codiverging with their vertebrate hosts for hundreds of millions of years.
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Herpes simplex research
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