The first Big News I remember was in 2015 from Albert Einstein College of Medicine

[sdl35]

Herpes Vaccine

Experimental Herpes Vaccine Upends Traditional Approach and Shows Promise

March 10, 2015—(BRONX, NY)—Scientists at Albert Einstein College of Medicine of Yeshiva University have designed a new type of vaccine that could be the first-ever for preventing genital herpes—one of the most common sexually transmitted diseases, affecting some 500 million people worldwide. By using a counterintuitive scientific approach, researchers were able to prevent both active and latent infections caused by herpes simplex virus type 2 (HSV-2), the virus that causes genital herpes. Findings from the research, conducted in mice, were published today in the online journal eLife. 

"Developing a herpes vaccine is one of the holy grails of infectious disease research," said co-study leader William Jacobs Jr., Ph.D., a Howard Hughes Medical Institute Investigator and the Leo and Julia Forchheimer Chair in Microbiology & Immunology at Einstein. "We decided to take an approach that runs counter to most of the tactics used by other scientists—and we seem to have cracked the code." Dr. Jacobs is also professor of microbiology & immunology and of genetics at Einstein.

It was generally assumed that an effective HSV-2 vaccine must stimulate the body to produce neutralizing antibodies—particularly against a viral surface protein called glycoprotein D (gD-2) that HSV-2 uses to enter human cells. A protein that triggers antibody production is called an antigen. For decades, researchers have focused on "subunit" herpes vaccines that rely primarily on gD-2 as the antigen to stimulate the body's antibody response––but none has prevented HSV-2 infection in humans. 

"This suggests we've been stimulating production of the wrong type of antibodies," said co-study leader Betsy Herold, M.D., the Harold and Muriel Block Chair in Pediatrics at Einstein and chief of the division of pediatric infectious diseases at the Children's Hospital at Montefiore and Einstein. Dr. Herold is also professor of pediatrics, of microbiology & immunology, and of obstetrics & gynecology and women's health at Einstein.

The Einstein team took a completely different approach in designing their "live" HSV-2 vaccine. Instead of using gD-2 to stimulate antibodies, they deleted the gene for gD-2 from the virus (and, consequently, the protein's expression on the viral surface) —a manipulation that weakens the virus, rendering it unable to infect cells or cause disease. They hypothesized that this altered virus would stimulate the body to produce different and more effective antibodies.

"We had a hunch that gD-2 might be masking other viral antigens, and that by removing this dominant protein we would expose those previously masked antigens to the immune system," said Dr. Jacobs.

When the vaccine, dubbed "delta-gD-2" ("delta" is shorthand for a gene deletion) was given to mice, it provided complete protection against subsequent infection with normal (wildtype) HSV-2, whether animals were challenged intravaginally or through the skin. No virus was detected in vaginal or skin tissue of vaccinated mice or in neural tissue, where HSV-2 often hides in a latent form only to emerge later to cause disease. When unvaccinated mice were challenged with wildtype HSV-2, all showed evidence of the virus in the three tissue sites, and all succumbed to the disease.

The vaccinated mice showed low levels of neutralizing antibodies but high levels of antibodies associated with a different immune response called antibody-dependent cell-mediated cytotoxicity (ADCC). This and other experiments described in the paper—such as finding that blood serum from vaccinated mice was able to passively protect unvaccinated mice —conclusively demonstrated that ADCC antibodies were responsible for protecting against HSV-2.

"Our findings challenge the existing dogma that says an effective herpes vaccine must stimulate neutralizing antibodies against gD-2," said Dr. Jacobs. "It's almost as if the virus evolved gD-2 specifically to hide the other antigens. gD-2 turns out to be a Trojan horse that misleads the immune system." 

The new vaccine also appears to be safe. The researchers calculated the number of wildtype viruses needed to kill mice—and then administered 1,000 times that number of delta-g D-2 viruses to mice that lacked immune systems and so couldn't ward off infections. The result: The mice survived and didn't develop herpes. The Einstein team hopes to begin clinical trials on humans within a few years.

Initial tests suggest that the vaccine is also effective against HSV-1, or oral herpes, although this needs to be further evaluated. In addition, the vaccine's novel design may help in creating vaccines against other disease-causing microbes that invade the body through mucosal tissues, including HIV and the bacterium that causes tuberculosis. "Genital herpes infections can not only be serious in and of themselves, but they also play a major role in fueling the HIV epidemic," said Dr. Herold. "People infected with HSV-2 are more likely to acquire and to transmit HIV—which further underscores the need to develop a safe and effective herpes vaccine."

Albert Einstein College of Medicine has filed patent applications related to this research and is seeking licensing partners able to further develop and commercialize this technology. Interested parties can contact the Office of Biotechnology at biotech@einstein.yu.edu.

The paper is titled "Herpes simplex type 2 virus deleted in glycoprotein D protects
against vaginal, skin and neural disease." The other contributors are: Christopher Petro, Ph.D., Pablo A. González, Ph.D., Natalia Cheshenko, Ph.D., Thomas Jandl, Ph.D., Nazanin Khajoueinejad, Angèle Bénard, Ph.D., and Mayami Sengupta, Ph.D., all at Einstein.

The study was support by grants from the National Institute for Allergy and Infectious Diseases, part of the National Institutes of Health (AI065309, AI03461, AI084225 and AI063537) and the Howard Hughes Medical Institute.

The authors declare no financial conflict of interest.

 

http://www.einstein.yu.edu/news/releases/1076/experimental-herpes-vaccine-upends-traditional-approach-and-shows-promise/

[Sanguine108]

Here's what they've published since then.   I need to check if they've done anything since this, too.

HSV-2 ΔgD elicits FcγR-effector antibodies that protect against clinical isolates

Christopher D. Petro,^1,2,3 Brian Weinrick,^1,2 Nazanin Khajoueinejad,³ Clare Burn,^1,3 Rani Sellers,⁴ William R. Jacobs Jr,^1,2and Betsy C. Herold^1,3

First published August 4, 2016 ; Received: May 10, 2016 ; Accepted: June 30, 2016
http://insight.jci.org/articles/view/88529

[Cas9]

10 hours ago, Sanguine108 said:

Here's what they've published since then.   I need to check if they've done anything since this, too.

HSV-2 ΔgD elicits FcγR-effector antibodies that protect against clinical isolates

Christopher D. Petro,^1,2,3 Brian Weinrick,^1,2 Nazanin Khajoueinejad,³ Clare Burn,^1,3 Rani Sellers,⁴ William R. Jacobs Jr,^1,2and Betsy C. Herold^1,3

First published August 4, 2016 ; Received: May 10, 2016 ; Accepted: June 30, 2016
http://insight.jci.org/articles/view/88529

I'm familiar with this study. Unfortunately they are still pre-clinic. It'll probably be another couple of years before they start animal studies.
The virus is very clever, and requires a clever approach to overcome it. This looks promising due to it's uniqueness and results. Of course what is successful in one organism is not necessarily successful in another.

If it works, the concern about passing on to others goes away. Huge!

[Sanguine108]

"The broad protection observed here in skin and vaginal models combined with the sterilizing immunity, as evidenced by absence of latent virus, support further development of the ΔgD-2 vaccine. To date, ΔgD-2 has protected 180 mice from lethal challenge (100%) and 94 of 95 mice from latency, as measured by qPCR for viral DNA or ex vivo reactivation. "

[Cas9]

5 hours ago, Sanguine108 said:

"The broad protection observed here in skin and vaginal models combined with the sterilizing immunity, as evidenced by absence of latent virus, support further development of the ΔgD-2 vaccine. To date, ΔgD-2 has protected 180 mice from lethal challenge (100%) and 94 of 95 mice from latency, as measured by qPCR for viral DNA or ex vivo reactivation. "

The one mouse that wasn't successful must of had an immune system problem. Poor bastard.

[sdl35]

Thank you for the responses. I had not seen the newer information. This would make life a lot better for most of us it sounds like.

It did read as though your partner would need to get a specific type of the HSV vaccine for your particular strain or type of HSV. Did you get the same impression? A custom vaccine for your particular strain?

Hopefully they could mass produce all the different strains out there to suit the different types.

And from there it's monogamy for us!

[Sanguine108]

5 hours ago, Cas9 said:

The one mouse that wasn't successful

yeah, makes me wonder if it was more of human error.

Once upon a time ago I worked in a lab and there was a test that took 5 days to complete.  One of the more time demanding steps called for pipetting ~1-2hrs under a flow hood.  One week I was tired, was a bit sloppy during this important step and come the 5th day I have wacky data that makes no sense.  The whole week down the toilet.  Learned my lesson and it never happened again but what a shit feeling to produce nothing for 5 days of work.  Other departments had robots but not mine.  Anyhow, I can only imagine treating 95 mice that some human error may occur so that 1 mouse does get infected.

1 hour ago, sdl35 said:

It did read as though your partner would need to get a specific type of the HSV vaccine for your particular strain or type of HSV. Did you get the same impression? A custom vaccine for your particular strain?

They tested the vaccine against several different strains of HSV.  
-Two strains of HSV-1 
-Three strains of HSV-2

"To assess whether ΔgD-2 protected against the different isolates,... mice were primed and boosted with ... ΔgD-2 (or VD60 lysate as the control immunogen) and then challenged with an LD90 dose of the 4 more virulent clinical isolates (Table 1) using the skin scarification model. All ΔgD-2–vaccinated mice survived challenge. While some mice exhibited mild epithelial disease, which peaked on day 4, the majority of animals had fully recovered by day 8 after challenge (Supplemental Figure 4, A and B). No signs of neurological disease were detected in any of the mice at any time point."

[sdl35]

That sounds like more of a comprehensive vaccine for many types. That is really something to look forward to!

Between this and Rational Vaccines we have some very promising options to wait for. 

I only wish it could be fast tracked for all the suffering this entity causes.

Thank you for clarifying, Sanguine108.

[Voyager2]

In their original March 2015 paper, they described mouse experiments and stated "we hope to begin clinical (human) trials in a few years."

Eighteen months later, in August 2016, they described further mouse testing, e.g., with different doses, and stated, "the protective effect of Delta gD-2 against a broad array of HSV-1 and HSV-2 clinical isolates differentiates it from other candidate vaccines."

This is a live vaccine that is clearly being developed as a prophylactic vaccine for uninfected people. Testing as of August 2016 showed it to be performing flawlessly.

It is now April 2017. Based on the two published papers, I would think/hope they are very, very close to human testing. Let's hope the vaccine continues to perform well and that the FDA consequently fast tracks it. Such a vaccine would protect an uninfected partner. That would be a game changer.