Cmv virus and blood pressure

According to recent figures from the American Heart Association, one in three U. Some cases of hypertension might be treated or prevented by antiviral therapy or a vaccine against CMV. Cytomegalovirus affects upwards of 99 percent of adults worldwide. Trending Omicron could peak in U. Turns out smarter kids are made, not born. Up Next. Under these circumstances, the immune system becomes busy keeping CMV at bay, which leads to an expansion of the T cells pool that is directed towards CMV.

At cost, the naive T cell pool decreases and makes it more difficult for older CMV positive individuals to generate an adaptive immune response to combat new infections, such as the novel SARS-CoV-2 virus. It has been estimated that CMV drives the attrition of the naive T cells pool by about 20 years [ 10 ]. The impaired immunity in CMV positive elderly individuals can also be caused by impaired cellular functions [ 11 ].

An active CMV infection will lead to immunosuppression via direct inhibitory effects on antigen presentation, NK, B and T cells responses, via sophisticated viral immune evasion strategies[ 12 ]. As a consequence, CMV associated immune senescence and immunosuppression in the elderly may increase their risk of dying from influenza and other infectious diseases [ 13 ], like SARS-CoV Considering the above circumstances, a vicious cycle may be generated, in which it would be difficult to determine what was the hen or the egg in this condition in relation to CMV.

Will elderly with an impaired and exhausted immune response reactivate CMV and maintain a low-grade chronic infection, which further, through its negative effects of immune cells, impair the outcome of a SARS-CoV-2 infection? CMV is a herpesvirus that generally infects small children. It causes congenital infection in 0. For many years, CMV infection was not considered to cause any pathology in healthy people. The primary infection produces mild or no clinical symptoms but results in a life-long latent or persistent infection, from which reactivation may occur throughout life [ 22 ].

However, emerging evidence suggests that CMV is linked to cancer and chronic inflammatory diseases [ 26 , 27 ], including those associated with increased risk of COVID CMV reactivation is driven by immune activation and inflammation [ 28 , 29 ]. In organ transplant patients, the allogeneic immune reaction causes rejection and leads to CMV reactivation [ 30 ].

Their immunosuppression poses them at risk of developing clinical CMV disease. The lungs are a major reservoir for latent virus [ 32 ]. Lung transplant patients may develop life-threatening CMV pneumonia, mainly through immunopathologic mechanisms, which is often followed by bronchiolitis obliterans, lung fibrosis, and poor lung function chronic rejection in the lung graft [ 33 , 34 ].

CMV is often reactivated in heart transplant patients and can increase the risk of transplant vasculopathy and fibrosis, leading to poor heart function or occlusion of the blood supply to the heart [ 35 — 37 ].

CMV is also linked to posttransplant diabetes [ 38 ]. These complications are reduced in patients who receive antiviral prophylactics against CMV [ 39 , 40 ]. In immunocompetent people, CMV infection is associated with hypertension, deep vein thrombosis, diabetes, myocardial infarction, and stroke [ 41 — 43 ]. CMV proteins are detected in the vasculature in the absence of viremia, and represent one example of chronic CMV antigen stimulation of immune cells that could drive inflation.

In sepsis patients, a strong inflammatory reaction may reactivate the virus within 4—7 days [ 44 ]—about the same time required for CMV reactivation in vitro [ 45 ]. A higher viral load of CMV is associated with enhanced mortality, and randomised trials show a lower reactivation rate in patients who receive antiviral prophylaxis for CMV [ 47 ]. They would be expected to suppress or even kill T cells and natural killer cells; activate macrophages and neutrophils in a cascade of events leading to a point of no return from inflammation; and could then affect endothelial cells and thrombocytes to cause coagulopathy and thrombus formation—precisely as observed in COVID patients.

SARS-CoV-2 activates macrophages by establishing a vicious cycle of M1 type macrophage polarization that will promote reactivation of latent CMV and fuel further inflammation.

CMV induces COX-2 expression and production of prostaglandin E2 PGE2 [ 51 ], expression of 5-lipoxygenase [ 52 ], and production of leukotriene B4, both powerful inflammatory mediators that drive inflammation. This cytokine storm combined by a weakened interferon response seem to contribute to the severe forms of COVID disease [ 58 ].

Furthermore, CMV directly supresses T cells and natural killer cell functions, thereby helping the virus avoid immune-mediated elimination. As a result, control of latent CMV decreases, enhancing risk of reactivation and development of clinical CMV disease, as observed in immunosuppressed patients. In blood, there is often a more moderate drop in monocytes, eosinophils, and basophils—the most prominent infiltrating cells in the lungs of COVID patients.

Many of the infiltrating macrophages would carry in latent CMV to the lungs that would be reactivated by the ongoing inflammation. D-dimer and fibrinogen levels are usually high, and there is evidence that microthrombi formation is prominent in the lungs of COVID patients [ 62 ].

The coagulopathy is also associated with enhanced risk for stroke and myocardial infarction, which may be first symptoms of COVID in young people. CMV is linked to deep vein thrombosis, stroke, and myocardial infarction, and CMV-infected endothelial cells trigger microthrombi formation in vitro [ 63 ]. Is the immune system first suppressed to allow for establishment of a chronic CMV infection, which could further impair the immune response to other infections?

Or, will a reactivated CMV infection cause hyper inflammation and simultaneous immunosuppression and lead to high risk of severe COVID in a more acute phase, due to their similarities in immune activation pathways? Studies referred to indicate that this may be the case, and future studies should therefore search for CMV in COVID patients and address this question in more depth.

The diagnosis of CMV is easily missed in the ICU, as few doctors are aware of this existing problem and the high risk of CMV reactivation in patients with inflammatory conditions. Virus induced immune senescence in the elderly may involve CMV reactivation, and could with increasing age be detrimental. In one case report, CMV DNA was detected in nasopharangeal swabs by sequencing—an unlikely finding in an otherwise healthy individual CMV reactivation, colitis and hypovolemic shock was observed in a critically ill patient undergoing experimental treatment for COVID In studies of T cell activation to CMV peptides in vitro , there was a clear trend for enhanced activation of CD8 positive T cells from COVID patients as compared with T cells from controls [ 66 — 68 ], but too few individuals were studied to demonstrate a statistical significance.

A recent study used a machine learning based method to predict the risk of COVID severity in adults and found that CMV specific antibodies were the strongest predictors of infection risk [ 69 ].

The hospitalized patients also had a higher incidence of both CMV and HSV- infections, but they had a less strong antibody response. For people who have weakened immune systems, especially people who have had an organ, stem cell or bone marrow transplant, CMV infection can be fatal.

CMV spreads from person to person through body fluids, such as blood, saliva, urine, semen and breast milk. There is no cure, but there are medications that can help treat the symptoms. Most healthy people who are infected with CMV may experience no symptoms. Some experience minor symptoms. People who are more likely to experience signs and symptoms of CMV include:.

Most babies who have congenital CMV appear healthy at birth. A few babies who have congenital CMV who appear healthy at birth develop signs over time — sometimes not for months or years after birth. The most common of these late-occurring signs are hearing loss and developmental delay. A small number of babies may also develop vision problems.

The following signs and symptoms are more common in babies who have congenital CMV and who are sick at birth:. Most people who are infected with CMV who are otherwise healthy experience few if any symptoms.

When first infected, some adults may have symptoms similar to infectious mononucleosis, including:. If you have CMV but are otherwise healthy, and you're experiencing any mild, generalized illness, you could be in a reactivation period. Self-care, such as getting plenty of rest, should be enough for your body to control the infection. If you know you were infected with CMV during your pregnancy, tell your baby's doctor.

The doctor will likely assess your baby for hearing or vision problems. When the scientists inactivated the virus through the use of ultraviolet light, renin expression did not increase, suggesting that actively replicating virus was causing the increase in renin. In their final experiments, the researchers demonstrated that the protein angiotensin 11 was also increased in response to infection with CMV. According to recent figures from the American Heart Association, one in three U.

Often dubbed "the silent killer," uncontrolled high blood pressure can lead to stroke, heart attack, heart failure or kidney failure, notes Crumpacker. Some cases of hypertension might be treated or prevented by antiviral therapy or a vaccine against CMV. Elizabeth's Medical Center, Boston. Note: Content may be edited for style and length.

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