Herpes is a terrifying “gift that keeps on giving” that can hurt to breathe…
< /p>
Have you been alive and well the day before, but the next day you have rashes and blisters on your waist that you can’t scratch, itchy and painful to the point of “crying father and mother”?
Are you often sleepless, upset, or too fucked（tan） When working （wan）, you find that the corners of your mouth are flushed, and small chickenpox grows on your lips, like “bamboo shoots after a rain”, until the scabs fall off?
Do you “think” you’ve cured the above annoying blisters every time, only to have it again years or even months later “Meet” until “reconciled” again…
If yes? Congratulations, you may have carried a low-key but not simple virus-herpes virus!
As one of the most prevalent viruses in humans, there are 8 types of herpes viruses: herpes simplex virus (HSV ) 1 and 2, varicella-zoster virus(VZV), Epstein-Barr virus( EBV), cytomegalovirus(CMV) and human herpesvirus(HHV)6, 7 and 8. According to the statistics of the World Health Organization(WHO), there are 3.709 billion people aged 0-49 in the world who are infected with HSV1 and cause oral herpes 67% of the population. In addition, 13.2% of the global population(about 490 million)infected with HSV2 causes genital herpes. Domestic studies have also reported that the cumulative incidence of herpes zoster in people aged 50 and over is 22.6/1000 (that is, about 23 out of 1,000 people aged 50 and over), and the incidence rate is increasing year by year. After the initial primary infection(usually mild or asymptomatic), the herpes virus tends to lie dormant in the host for life, waiting for The timing strikes again.
If you thought that a herpes infection was at most a few weeks of itchy, sore, “sour,” you’d be wrong. A recent study published in Diabetologia showed that herpes viruses are associated with the onset of prediabetes:Two common herpes viruses, herpes simplex virus type 2 (HSV2) and cytomegalovirus(CMV)may lead to impaired glucose metabolism in humans and significantly increase the risk of type 2 diabetes in infected individuals< span>(T2D) risk.
(Image credit: Diabetologia)
Pre-diabetes is a condition that usually precedes the onset of type 2 diabetes metabolic status, when an individual exhibits impaired fasting glucose(IFG)or impaired glucose tolerance(IGT) is diagnosed with prediabetes. A previous study found that the incidence of T2D in prediabetic patients (7.6% per person per year) was much higher than that in normal glucose tolerance patients(0.6% per person per year).
To investigate whether there is an association between latent herpesvirus infection and the development of prediabetes, researchers analyzed thousands of population health research platforms. health data of the subjects, and conducted from baseline(2006-2008)to follow-up(2013-2014) About seven years of tracking. They found that about 360 subjects developed markers of prediabetes. Interestingly, among the several herpesviruses examined, HSV2 and CMV were significantly associated with the incidence of prediabetes in individuals with normal glucose tolerance at baseline—compared with seronegative individuals, People with CMV were 33% more likely to develop prediabetes, while those infected with HSV2 were 59% more likely to develop prediabetes!
Herpesvirus positivity associated with prediabetes incidence /span>
(Image credit: Diabetologia)
Subsequently, the researchers identified many factors that may affect the development of diabetes (such as gender, age, BMI, education, smoking, physical activity, family history, Hypertension, blood lipid levels, insulin resistance, fasting, etc.) were taken into account, and a multivariate analysis was performed, and it was found that HSV2 and CMV consistently and complementarily promoted the development of prediabetes. In this regard, the researchers stated:“Previously, the incidence of prediabetes was largely attributable to age, BMI, cholesterol, and fasting blood glucose. However, the results of this study suggest that herpesviruses HSV2 and CMV can additionally increase prediabetes. risk of developing diabetes.”
about the two models in the logic Selected proportions of viral and confounding factors for (pre)diabetes incidence
(Image source: Diabetologia)
< p>Next, the researchers further analyzed the association between the herpes virus and diabetes mellitus commonly used indicator glycosylated hemoglobin(HbA1c) to more intuitively show the virus and diabetes Relationship. HbA1c concentration can effectively reflect the average blood glucose level in the past 8-12 weeks. The results of the study confirmed the researchers’ conjecture thatHSV2 was significantly associated with HbA1c levels, suggesting that virus carriers do indeed have long-term hyperglycemia. Moreover, this association was independent of other confounding factors and the prevalence of prediabetes itself.
Each herpes virus serostatus is associated with HbA1c separately
< p>(Photo credit: Diabetologia)
From this, researchers concluded that infection with certain herpes viruses may affect diabetes mellitus Occurrence and development play a role in promoting. Although several other known risk factors for diabetes, such as cholesterol and obesity, clearly play a larger role than the herpes virus in determining a person’s likelihood of developing diabetes, the new finding serves as a good cautionary tale :In the face of herpes virus, which is highly infectious and lifelong, people still need to invest more public health efforts to prevent infection – and the development of a herpes virus vaccine seems to be an effective a preventive tool and is expected to reduce the incidence of diabetes.
In fact, in addition to causing diabetes, with the in-depth study of herpes virus in recent years, people have gradually realized that herpes is also associated with diseases such as Alzheimer’s disease. The occurrence and development of stroke and cardiovascular disease are closely related. The findings have prompted accelerated research into vaccines for the herpes virus. The shingles vaccine that has been marketed is the best example. It is widely used by middle-aged and elderly people over 50 years old. It can reduce the risk of shingles in the elderly due to weakened immunity, and also help avoid other diseases of the elderly. occur. However, vaccines for several other herpesviruses are still in development. Therefore, it is of great significance for the development of vaccines to further understand the invasion mechanism of herpes virus and achieve precise “prescribed medicine”.
Coincidentally, researchers from Northwestern University Feinberg School of Medicine recently revealed a cunning strategy for the herpes simplex virus HSV to infect the nervous system. Opening a long-awaited path to vaccine development for HSV1 and HSV2.
(Image source: Nature)
p>
After a virus invades a cell, it relies on motor proteins to carry it to the nucleus, where it thrives; however, it is unclear how these molecular motors are manipulated by the virus. In this study, the scientists found thatviruses grab a motor protein in the first infected cell and turn it against it. When it comes to the next round of infection, let it lead the way.
Scientists first infected human retinal pigment epithelial cells with HSV1. They were pleasantly surprised to find that when normal epithelial cells were invaded by HSV1 virus, the virus Most of the capsid remains on the nuclear membrane, indicating that the virus has successfully entered the nucleus; but when the host epithelial cells lack kinesin, the viral capsid will accumulate in the cytoplasm, and the virus loses the ability to enter the nucleus.
HSV infected epithelial cells (Image source: Nature)
< p>
The second round of infection verification followed. This time, the team grew HSV1 viruses in epithelial cells lacking or not lacking kinesin, and then used these viruses to invade primary sensory neurons that had their own kinesin proteins. Surprisingly, viruses cultured in normal epithelial cells successfully entered the nucleus, while viruses assembled in kinesin-deficient epithelial cells rarely entered the nucleus.
This shows that the virus may take some kinesins of epithelial cells for its own use in the first round of infection, and then use it in the next round of infection.to invade neurons.
To test this conjecture, scientists made special replacements for kinesin in epithelial cells, and then administered a drug to neurons to carry the kinesin. The virus is “immobile” on the microtubule. Sure enough, the virus’s ability to infect neurons declined.
viral captured kinesins transport capsid to nucleus
(Image source: Nature)
This discovery provides a new idea for HSV vaccine development. As paper author Smith says, “By understanding how the herpes virus achieves this incredible feat to gain access to our nervous system, we can now think about how to remove this ability.If you Stop it from assimilating kinesin and you will keep the herpes virus from infecting the nervous system. You have a candidate for preventive vaccine development.”
The research and development of herpes vaccine is full of hope, although the road is long and difficult. I wish the readers here to stay away from this trouble and have smooth and blister-free skin~
References [1] Woelfle T, Linkohr B, Waterboer T, Thorand B, Seissler J, Chadeau-Hyam M, Peters A. Health impact of seven herpesviruses on (pre)diabetes incidence and HbA1c: results from the KORA cohort. Diabetologia. 2022 May 11:1–11. doi: 10.1007/s00125-022-05704-7.[2] Pegg CE, Zaichick SV, Bomba-Warczak E, Jovasevic V, Kim D, Kharkwal H, Wilson DW , Walsh D, Sollars PJ, Pickard GE, Savas JN, Smith GA. Herpesviruses assimilate kinesin to produce motorized viral particles. Nature. 2021 Nov;599(7886):662-666. doi: 10.1038/s41586-021-04106-w .
Writing | Le YiEditing | Swagpp
Click “Read the original text” below Download Metz Medical APP