Viruses

Viruses, ultraviolet sunlight increase skin cancer risk in posttransplant patients

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Among individuals who have undergone solid organ transplantation, viral infections and exposure to ultraviolet sunlight were associated with the highest risks for skin cancers, according to a study.

“Nonkeratinocyte skin cancers are an important cause of morbidity and mortality for immunosuppressed solid organ transplant recipients (SOTRs), but the spectrum of disease and risk factor characteristics are unknown,” Michael R. Sargen, MD, of the division of cancer epidemiology and genetics at the NIH National Cancer Institute, and colleagues wrote.

In the population-based cohort study, the researchers characterized the spectrum of disease and risk factors for common and rare nonkeratinocyte skin malignancies in a cohort of 444,497 solid organ transplant recipients in the United States.

Eligible participants had undergone procedures between Jan. 1, 1987, and Dec. 31, 2017. Risk was assessed using standardized incidence ratios (SIRs) compared with the general population.

Results showed that 2,380 nonkeratinocyte skin cancers from the transplant cohort underwent analysis. Patients had a median age of 50 years (range, 0-96) at transplant. The cohort was 61.7% men and 61.2% non-Hispanic white.

The most common malignancy was melanoma at 61.8%, followed by Merkel cell carcinoma at 14%, Kaposi sarcoma at 7.8%, sebaceous carcinoma at 7.1% and cutaneous lymphomas at 4.5%.

The highest risks were reported for cancers associated with viruses, according to findings. The highest virus-related malignancy risk was for Kaposi sarcoma (SIR = 20.5; 95% CI, 17.7-23.7), followed by Merkel cell carcinoma (SIR = 16.2; 95% CI, 14.5-18.1) and extranodal natural killer/T-cell lymphoma (SIR = 44.3; 95% CI, 5.37-160).

Sebaceous carcinoma risk was significantly elevated in the transplant setting (SIR = 15.2; 95% CI, 13-17.7), as was risk for anaplastic large cell lymphoma (SIR = 6.82; 95% CI, 4.53-9.85) and diffuse large B-cell lymphoma (SIR = 5.17; 95% CI, 3.28-7.76).

Men were at elevated risk for multiple skin cancer types. Older age at transplant was another risk factor for multiple cancers, as were factors associated with UV radiation exposure such as non-Hispanic white race and ethnicity, living in a place with elevated UV radiation exposure and diagnosis of keratinocyte carcinoma following transplantation. As time passed following transplantation, cancer risk also increased.

The main factor that reduced melanoma incidence was treatment with mammalian target of rapamycin inhibitors (incidence rate ratio = 0.75; 95% CI, 0.57-0.98), according to the results.

Of the malignancies that underwent analysis, 39.4% were head and neck disease.

“The findings of this cohort study suggest that viruses, UV radiation exposure and immunosuppression are associated with the development of skin cancer in SOTRs,” the researchers concluded. “Certain high-risk subgroups may benefit from increased skin surveillance, and treatment with mammalian target of rapamycin inhibitors could be effective for melanoma chemoprevention in the transplant population.”

Insane Numbers of Viruses Are Constantly Falling on Us From The Sky, Study Shows

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They’re all over the planetary boundary.

If there are viruses on the ground and viruses in the water, one might expect there are viruses in the sky as well.

And boy howdy are there ever. Scientists have just found that hundreds of millions of viruses per day are deposited above the lowest layer of the atmosphere.

This could explain a curious phenomenon – how almost identical viruses end up at wildly distant geographical locations and varying environments.

Of all the microbes on the planet, viruses are the most abundant, with an estimated nonillion (10^30) in the ocean alone. And of course we know viruses can be airborne – that is one of their major transmission methods.

Previously, the USDA Forest Service established that over a trillion viruses per square metre rains down every year.

That, as it turns out, is a conservative figure.

“Every day, more than 800 million viruses are deposited per square metre above the planetary boundary layer – that’s 25 viruses for each person in Canada,” said University of British Columbia virologist Curtis Suttle.

He’s one of the senior authors of a new study that, for the first time, quantifies the number of viruses being swept up into the free troposphere above the lowest layer of the atmosphere – the planetary boundary layer where all the weather happens, but below the stratosphere, where planes fly.

“Roughly 20 years ago we began finding genetically similar viruses occurring in very different environments around the globe,” he said.

“This preponderance of long-residence viruses travelling the atmosphere likely explains why – it’s quite conceivable to have a virus swept up into the atmosphere on one continent and deposited on another.”

The aerosolisation mechanisms of viruses – how they get airborne – are not well understood, but studies have suggested that, at least in some cases, they are swept up into the atmosphere mixed with dust and sea spray. We know bacteria are dispersed this way, so it makes sense that viruses can be, too.

Suttle and his team wanted to know exactly how many viruses were being transported to the altitude of 2,500 to 3,000 kilometres (1,550 to 1,860 miles).

They installed two collectors on platforms above the planetary boundary layer in Spain, in the Sierra Nevada Mountains, a region under the influence of a global dust belt.

They found that there were millions of bacteria and billions of viruses being deposited per square metre per day in the free troposphere.

The deposition rates for viruses were 9 to 461 times higher than the deposition rates for bacteria.

That doesn’t mean the situation is dire – obviously we’ve been living with it just fine, and whether or not a virus can survive in a new ecosystem depends on whether there’s a suitable host.

However, they can survive atmospheric transport, so there is a possibility that they can have an effect on a new ecosystem.

Viruses also aren’t just pathogens. Recent evidence suggests they play a key role in the ocean’s carbon cycle. There are also viruses called bacteriophages that help humans by killing harmful bacteria.

Dispersing in the atmosphere and staying there for a long time, the team writes in their paper, provides a mechanism of preserving the diversity of viruses, much like a sort of “seed bank.”

“Significant downward fluxes of bacteria and viruses from the atmosphere may have effects on the structure and function of recipient ecosystems,” they wrote.

“Rather than being a negative consequence, this deposition provides a seed bank that should allow ecosystems to rapidly adapt to environmental changes.”

Their research has been published in the International Society for Microbial Ecology Journal.

Viruses’ Fight One Another in their Own Biological WarFare

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Viruses latch on to a cell, setting off a competition for a successful infection. 

Just like animals compete with one another throughout evolution, as suggested by Darwin’s theory, so do organisms. They may be tiny, but they can still do a lot of damage as they fight one another for resources and try to kill off any competition. The same goes for viruses as well. Some of these infect just a single species of bacteria, and many of them consist of genes that can stop the competition from infecting their host.

Viruses vary in just how much damage they can do. While some of them simply spread in their hosts soon after an infection, others are slightly more devious in the way they infect their victims. These will bury themselves deep into the host’s genome, keeping hidden for many generations. In doing this they’re able to infect far more people over a greater time period. But there are also disadvantages for the virus in doing things this way. One being that if they remain hidden for too long, another virus may just come along and destroy the host. It’s for that reason that researchers believe that viruses use some form of biological warfare to ward off future invaders.

To get to the bottom of this virus competition researchers set out to sequence various single bacterial specials samples. They discovered that many of these genomes had viruses integrated within them and a closer look at the genes revealed that they had a variety of means for destroying fellow viruses. One of these involved using certain elements from bacteria to protect themselves, while others had proteins that were able to stop any viruses from entering the cell or that stick to other viruses’ DNA to stop it from producing proteins. But, the system that was the most elaborate was where a virus called Phrann that encodes proteins to signal when there’s a shortage of amino acids. It then shuts down the bacteria’s metabolism until amino acid levels are back to how they should be. It also encodes a different protein that stops any manufacturing from taking place until a new virus comes along that it has to fight.

From Foe to Friend: Viruses Show New Promise as Cancer Treatment .

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Almost as long as scientists have known of the existence of viruses, they’ve dreamed of using the tiny pathogens as a weapon against cancer. Now, as a result of advances in genetic engineering and insights into the workings of the immune system, science is giving substance to the dream.

A variety of studies over the past few years have demonstrated the ability of specially modified viruses to attack and kill cancer cells – in the laboratory and, very recently, in some patients. Techniques vary from study to study, but the basic approach is to inject the viruses directly into tumors – allowing the virus to infect and kill many of the cancer cells and, equally important, to stimulate the immune system to launch its own assault on the tumor.

One high-profile example of this approach, reported recently on CBS News’ “60 Minutes,” involved researchers at Duke University who treated patients with glioblastoma with a modified polio virus. In a small, early study, 11 of 22 patients showed substantial improvement from the regimen.

Other research attracting journalistic attention is a clinical trial at the Mayo Clinic that uses the measles virus to treat patients with multiple myeloma. Investigators found that after infecting cancer cells, the virus causes them to clump together and disintegrate. The wreckage may trigger an immune system response that can prevent the disease from returning for a long period of time, researchers have suggested.

At Dalhousie University in Halifax, Nova Scotia, scientists have shown that reoviruses – common, benign viruses often found in the respiratory tract – can be engineered to specifically infect melanoma cells. The infection appears to prompt an immune system attack that kills not only the infected cells but also the uninfected cancer cells nearby. In early-stage clinical trials, the treatment has been shown to be effective in some patients with melanoma and, when coupled with chemotherapy, in some patients with head and neck cancers.

“There have been efforts to use viruses in cancer therapy for more than 50 years, but we now have more of a grasp of what’s going on, and why some viruses work better than others,” says Harvey Cantor, MD, chair of Dana-Farber’s Department of Immunology and AIDS. A key component to this understanding, Cantor says, is that the impact of the virus should not only kill the tumor cells, but it should also initiate a T cell immune response that destroys the primary tumor as well as metastases.

Cantor says researchers are also looking at combining this treatment approach with immune-checkpoint inhibitors, which can help “take the brakes off” the immune system and enhance the patient’s anti-tumor response.

“It’s a treatment concept that is very interesting and certainly has a lot of promise,” Cantor says.