Hi everyone. I'm Jeremy and I'm a single father of two daughters living in Utah and am 40 years old. I kissed a girl on a date a couple months ago and little did I know that she had oral hsv1, though I didn't know what it was at the time. I later saw her and she had a cold sore, which I asked her about. By that time, I had researched what was going on with me as I had my primary outbreak on Jan 1 (what a way to welcome the new year) for about a week.
I know that my two daughters don't have the virus as I've tested negative for it in the past (I tested positive at 1.0 iGG this past week) and my ex-wife is also negative. So I'm pretty concerned about the likelihood I can transmit this to them. I've had 4 or so very minor breakouts since January 1st - a pimple on the lip, mustache area, one small one on my chin. My outbreaks seem to be about once or twice a week and started in early February and are very minor so far, but every few days it feels like there is slight tingling and some pain in my mouth area.
My question is, for my daughters who don't have this virus, can I hug them? How should I cook for them? I am washing my hands regularly and always checking my face... Besides just very careful hygeine, what are the chances I could pass this on to my daughters? It's my primary concern not do to that. Also, the outbreaks are happening regularly and I'm eating pretty healthily. I'm aware of L-Lysine and the arginine ratio of foods. I drink a lot of water, take supplements. I heard over time, the outbreaks become less frequent/severe.
Been having a hard time psychologically with this. I know there's much worse things that can happen, but I'm feeling pretty depressed and can't bear the thought of my daughters getting this (they are 10 and 7).
I am really pissed off that my partner's mum kissed me on the cheek twice with a healing cold sore.
Here we all are on this forum trying to educate ourselves as much as possible about this virus, agonising over how to protect partners, and even debating whether we can embark on a relationship ever again and yet this person with a cold sore is so ignorant and uneducated that they will put someone else at risk by initiating skin to skin contact with an active infection.
I know she probably thinks nothing on it and almost certainly has no knowledge of asymptomatic shedding, but surely the very least she could do is be mindful of contact with people while she has a full blown sore.
I don't care that oral hsv1 is very common. I already have hsv2 and don't want hsv1 as well (yes I have heard that it's hard to get hsv1 with a preexisting hsv2 infection but she doesn't know what I have or don't have.
Perhaps it's irrational given the fact it was only my cheek. But it's the lack of thought that incenses me, while I have stressed over this every day since getting it.
Is thia herpes? I notice this for a week after suspected exposure. (Kissing) or am I overthinking?
my lips sometimes itch but the white spots doesnt hurt.
Exploring how herpes simplex virus changes when passed between family members
October 20, 2017
A new study explores how herpes simplex virus might change when passed from one individual to another, information that may prove useful in future development of therapeutics and vaccines. This rare glimpse into a transmission event reveals nearly perfect genetic transmission of the virus from a father to his son and lays the foundation for future studies exploring the genetic diversity of this virus. A paper describing the study appears online Oct. 20 in the journal Scientific Reports.
“Millions of people worldwide have herpes simplex virus,” said Moriah Szpara, assistant professor of biochemistry and molecular biology at Penn State and an author of the paper. “We see locally distinct variants of the virus with distinct genetic fingerprints in different regions around the world, and, with the prevalence of international travel, we’re starting to see a lot of different variants of the virus appearing in one place. This could have implications for how the virus evolves and how we design therapeutics to combat it. Studies of a related virus — human cytomegalovirus — suggest that the virus diversifies after transmission, and we wanted to see if this was also the case for herpes simplex virus.”
Herpes simplex virus type 1 (HSV-1) is a highly contagious infection that commonly causes oral and genital lesions. More severe symptoms can also occur, such as eye disease and, in rare cases, encephalitis -- inflammation of the brain that can cause flu-like symptoms, confusion, seizures, or problems with movement. Although some medications can reduce the severity and frequency of the symptoms, there is no cure for HSV-1 and no guaranteed way to prevent transmission. HSV-1 can be transmitted through contact with sores or saliva around the mouth — as is often the case in familial transmission — or sexually.
“Capturing transmission of herpes simplex virus is incredibly difficult,” said Szpara, “in part because the social stigma associated with having the virus makes it unlikely for sexual partners to admit when they transmit it. The virus also lasts a lifetime. Unlike the flu, which comes and goes, HSV remains in an individual’s body for the remainder of their life. Periods of latency and reactivation make it hard to know exactly when the virus was first transmitted.”
“In this study, we had a known case of familial transmission,” said Nancy Sawtell, professor at the Cincinnati Children’s Hospital Medical Center and an author of the paper. “Samples from a father and son were cultured in the lab, enabling us to investigate potential differences of the virus after transmission. To gain a comprehensive look at the results of transmission, we used genetic sequencing, and we examined each virus in an animal model to compare the level of virulence, or the ability to cause disease. Animal models have the ability to reflect the interactions of all the body’s systems at once — the outer surface, the immune system and the nervous system all interact during the response to herpes simplex virus infection.”
Genetically, the viruses taken from the father and son were a near-perfect match. The viruses also had similar pathology when tested in mice — they grew at a similar rate and had a similar ability to set up long-term infection in the brain. Although the viruses from the father and son were not completely identical, these results suggest that HSV-1 may not change much when transmitted between closely related individuals. However, the researchers suspect that transmission between unrelated hosts may provide a more dramatic opportunity for change.
“An individual’s immune system exerts selection pressure on a virus,” said Utsav Pandey, graduate student at Penn State and first author of the study. “The son got at least half of his immune system from his father, so it was probably a similar selective environment. Unrelated individuals likely differ more in their immune system, which could shape the virus.”
The research team also compared the performance of the viruses from the father and son to two separate clinical cultures of HSV-1. The variants from the father and son were less virulent — less severe — when tested in mice. Additionally, the genome sequence of the viruses in the father and son, who were from the United States, did not fit in as expected with other HSV-1 genomes that have been genetically sequenced from the United States or Europe.
“This study broadens our knowledge of what herpes simplex virus variants are circulating in the U.S.,” said Szpara. “It’s not just the United States/European variants that are used in vaccine development and clinical studies. When we think about designing therapeutics and vaccines, we need to know how the virus can differ or we may design something that only controls the virus from a particular region.”
To further understand how genetic diversity of HSV-1 is generated, the researchers plan to turn their attention to studying transmission of the virus between unrelated individuals. “If we could understand how much the virus changes when passed between unrelated individuals and how the virus’ genetics influences the level of virulence or level of harm the virus can do,” said Szpara, “then hopefully we can design better treatments for HSV-1.”
In addition to Szpara, Sawtell, and Pandey, the research team includes Daniel Renner, computational scientist at Penn State; and Richard Thompson, professor of molecular genetics, biochemistry, and microbiology at the University of Cincinnati. The work was funded by the National Institutes of Health and the Pennsylvania Department of Health Commonwealth Universal Research Enhancement (CURE) program and supported by the Huck Institutes of the Life Sciences at Penn State.