How infection site affects the immune system

A new study by scientists at the Gladstone Institutes shows that infection sites could affect the immune system's response to a virus and the way the virus spreads through the body. The researchers focused on common routes of sexual transmission of viruses, such as the lower female reproductive tract and the lower gastrointestinal tract that includes the large intestine and the anus.

These mucosal barriers-the body's openings lined with a membrane called mucosa are responsible for distinguishing between harmless bacteria that normally reside in human and potentially dangerous pathogens, as well as other substances, such as food or sperm. Human body is constantly trying to balance between tolerating harmless elements and defending against the threats.

Reseachers discovered that the body's reaction is different based on the infection site. They showed that the vaginal and rectal cavities activate a distinct immune response to the same pathogen. To conduct the study, research team created a new model of viral infection through the rectum that uses lymphocytic choriomeningitis virus (LCMV), a rodent virus often used in research to model other pathogens. They then compared their findings to their previous work on vaginal infection by LCMV.

In 2016, they showed that vaginal infection causes a delayed response by protective cells. As a result, the immune system takes longer to clear the virus from the female reproductive tract. They also noticed that the virus stayed in the vagina and didn't spread to other parts of the body. In contrast, the new study indicates that, after infection through the rectum, the virus rapidly spreads throughout the body. The scientists also found that the virus wasn't being carried through the blood. Instead, LCMV infects the body's own immune cells, which in turn spread the virus systemically. Interestingly, this is the same dissemination process used by the HIV virus.

The initial immune response elicited depends on the route of infection, and can actually dictate the dissemination of the virus. The researchers revealed that mucosal barriers have different tolerance mechanisms that affect the immune system's response to invading pathogens. Once a virus breaches one of the barriers, early events in the body's response to that virus can play a key role in determining the outcome of an infection.
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Cancer-killing virus alerts immune system

A new UC San Francisco study has shown that a cancer-killing ("oncolytic") virus currently in clinical trials may function as a cancer vaccine-in addition to killing some cancer cells directly, the virus alerts the immune system to the presence of a tumor, triggering a powerful, widespread immune response that kills cancer cells far outside the virus-infected region.

Using novel approaches to examine exactly how oncolytic viruses attack tumors, issue of Cancer Research provided surprising insights about how a viral infection can cooperate with the immune system to attack cancer cells. The study highlights an opportunity to combine this form of therapy with cancer immunotherapy drugs such as checkpoint inhibitors, which unleash the immune system's full cancer-fighting power.

The idea that viruses could fight cancer goes back to the early 20th century, when doctors noted that cancer patients sometimes experienced dramatic remission after getting viral infections. Researchers have been developing oncolytic viruses since the 1980s, but following the U.S. Food and Drug Administration's 2015 approval of Amgen's Imlygic (T-Vec) as the first oncolytic viral therapy in the U.S., such viruses have become a closely watched area of therapeutic development.

Viruses appear capable of attacking tumors in a number of different ways by directly infecting them, by releasing tumor proteins that trigger a broad immune response against the cancer, and by damaging the blood supply tumors need to survive. To better understand the underlying mechanisms of these viral therapies, a collaboration was forged between UCSF vascular researcher Donald McDonald, MD, Ph.D., and researchers at San Francisco-based biotech SillaJen Biotherapeutics Inc. (formerly Jennerex Biotherapeutics, Inc.)

SillaJen is developing an oncolytic viral therapy called Pexa-Vec, currently in phase III and phase Ib/II clinical trials for use against primary liver and colorectal cancers, respectively. Pexa-Vec is an engineered virus based on the harmless vaccinia cowpox virus, also the basis for the original smallpox vaccine. Early observations suggesting that the virus might attack cancer in part by damaging blood vessels that feed tumor growth.

To study how the modified virus attacks tumors, researchers in the McDonald lab injected it intravenously into mice genetically modified to develop neuroendocrine pancreatic cancer. They found that the virus failed to infect healthy organs or make the animals ill, but succeeded in infecting blood vessels within tumors. These initial infections caused the vessels to leak and expose the tumor cells to the virus. In these experiments, the virus managed to infect and destroy only a small proportion of tumor cells directly, the researchers found, but within five days of the initial infection, the rest of the tumor began to be killed by a powerful immune reaction.

At first small spots of the tumor were infected, but then most of the tumor started to die. The researchers found that by killing some tumor cells directly, the viral infection exposed tumor proteins that could be detected by the immune system, triggering an immune attack on the rest of the tumor. The researchers demonstrated this by temporarily getting rid of the immune system's cancer-killing cells, called CD8+ or cytotoxic T cells, and showing that without these cells, the virus killed only the initial five percent of cancer cells.

When the researchers examined the tumors, they discovered that the second drug acted by making the immune system hyper-alert to tumor proteins released by the viral infection, rather than through effects on tumor blood vessels. This finding suggests that pairing Pexa-Vec's ability to awaken the immune system to previously ignored signs of cancer with the newest generation of checkpoint inhibitors, which act by unleashing the immune system's full force, might be an extremely potent combination therapy.
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Virus cracking molecules for treating Hepatitis B

Indiana University researchers have made an important step forward in the design of drugs that fight the hepatitis B virus, which can cause liver failure and liver cancer. ''The drug could attack hepatitis B virus on multiple fronts-preventing replication and killing new copies of the virus," said senior author Adam Zlotnick, a professor in the IU Bloomington College of Arts and Sciences' Department of Molecular and Cellular Biochemistry.

A virus reproduces by hijacking a host's cellular machinery to produce more of the virus. The majority of viruses protect their genetic material-DNA or RNA-inside a protein shell called a "capsid." The research leads to discovery of  a class of molecules called core protein allosteric modulators, or CpAMs, that disrupt capsid protein assembly.

CpAM molecules attack viruses by causing their shells to assemble incorrectly, interrupting the life cycle of the virus. Previously, CpAMs were seen as only able to disrupt a virus during formation of the capsid, after which its DNA was protected inside a hard casing.

To make their discovery,  researchers bound the CpAM to a chemical called TAMRA-a crimson-colored dye used in some red lipstick-to make it fluorescent and easier to detect in experiments. Using cryo-electron microscopy, they found the small CpAM molecule could make the large, soccer ball-shaped virus capsid bend and distort.

The big implication is viral capsids aren't as impenetrable,  if this type of interference works against hepatitis B virus, it might also work against other viruses. About half of known virus families have soccer ball-like capsids; examples include polio and herpes.  This study may lead to better treatments against them since the mechanisms behind capsid disruption could lead to drugs against any of them.
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How intestine repairs itself

Researchers at Baylor College of Medicine, Johns Hopkins University School of Medicine and the University of California, San Francisco have gained new insights into how the small intestine, one of the fastest renewing tissues in the human body, repairs itself after injury caused by intestinal rotavirus infection. Their findings have led them to propose that, contrary to the current thinking, how the intestine repairs itself seems to depend on the type of damage, and they found that triggers that were previously thought to be unimportant are actually essential for repairing virus-caused injury.

They studied different damage model, damage caused by rotavirus, a common small intestinal viral infection that affects young children. Repair and turnover of the epithelium, the most external cellular layer of the small intestine responsible for absorption of nutrients and other functions, depend on the intestinal stem cells, regardless of the cause of the damage. There are two types of intestinal stem cells: CBCs (crypt-based columnar cells) and reserve intestinal stem cells. The type of injuries studied until now damages the highly proliferative CBCs, and when these stem cells are destroyed, the reserve intestinal stem cells respond to restore the damage. The response to injury caused by rotavirus, however, is different.

Rotavirus is an infection and has a very specific damage pattern, the virus specifically infects epithelial cells, but not the stem cells. The first finding refers to the type of stem cell involved in the repair of the epithelial cells damaged by the virus. Previous studies had shown that when CBC stem cells are damaged, the reserve stem cells come to their rescue leading the reconstitution of the damaged epithelium. When rotavirus damages the epithelium, but not the stem cells,  the CBCs, not the reserve stem cells, are the primary cell type involved in the restoration of the intestinal epithelium.

 CBCs were not considered important for the repair of intestinal epithelium, but the results show that they are crucial for injury repair after rotavirus-induced epithelial cell damage in contrast to previous studies supporting the reserve intestinal stem cells as the cell type involved in epithelial restitution. The second finding refers to the source of the signaling molecules-called WNTs that trigger the growth and activation of stem cells leading to injury repair. Scientists have described two sources of WNT molecules, epithelial cells and mesenchymal cells. Epithelial WNT molecules were essential to signal the stem cells to repair the damage caused by rotavirus infection.
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Protein-like virus essential for memory

A protein involved in cognition and storing long-term memories looks and acts like a protein from viruses. The protein, called Arc, has properties similar to those that viruses use for infecting host cells, and originated from a chance evolutionary event that occurred hundreds of millions of years ago.

The prospect that virus-like proteins could be the basis for a novel form of cell-to-cell communication in the brain could change our understanding of how memories are made, according to Jason Shepherd, Ph.D., a neuroscientist at University of Utah Health.

Researchers suspected that something was different about Arc when his colleagues captured an image of the protein showing that Arc was assembling into large structures. With a shape that resembles a capsule from a lunar lander, these structures looked a lot like the retrovirus, HIV. Prior work had shown that mice lacking Arc forgot things they had learned a mere 24 hours earlier. Further, their brains lacked plasticity.

 There is a window of time early in life when the brain is like a sponge, easily soaking up new knowledge and skills. Without Arc, the window never opens. Scientists had never considered that mechanisms responsible for acquiring knowledge could stem from foreign origins.  A protein important for cognition and memory named Arc can encapsulates genetic material (polyhedron enveloping the ribbon-like strands) and delivers it to brain cells in a manner similar to the way in which viruses infect host cells.

Seeing Arc's unusual propensity to form virus-like structures prompted researchers to scrutinize the protein sequence with a new set of eyes. They found that regions of the code were similar to that from viral capsids. An essential tool for viral infection, capsids carry virus' genetic information and deliver it from cell to cell in its victim.

Given that Arc looks like a viral protein, Shepherd and his colleagues designed a set of experiments to test whether it also acts like one. They first determined that several copies of Arc self-assemble into hollow virus-like capsids and stash its own genetic material, in this case mRNA, inside them. When the scientists added the capsids to mouse brain cells, or neurons, growing in a dish, Arc transferred its genetic cargo into the cells.

After viruses invade host cells, they emerge ready to infect once again. It appears that Arc works in a similar way. The scientists gathered Arc that had been released from mouse neurons and determined that the proteins and their cargo could be taken up by another set of neurons. Unlike for viruses, activating neurons mobilizes Arc, triggering the release of capsids.

A protein involved in cognition and storing long-term memories looks and acts like a protein from viruses, according to research by scientists at University of Utah Health. The protein, called Arc, has properties similar to those that viruses use for infecting host cells and could be the basis for a novel form of communication in the brain. An ancestor to retroviruses, called retrotransposons, inserted its genetic material into the animals' DNA, the event led to the mammalian. The significance of such an event is hinted at by the fact that it happened more than once.
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Gene therapy may kill HIV

Gene therapy may have the potential to eradicate HIV in people infected with the virus, new animal research suggests. The science centers around the use of "chimeric antigen receptor" (CAR) genes. In laboratory work with monkeys, these engineered cells have destroyed HIV-infected cells for more than two years, scientists reported.

T-cells are the cells that are largely responsible for human ability to fight off pathogens and get rid of infections in the body. Every T-cell has a unique receptor, or molecule, on it. That receptor allows the cell to recognize a specific target-a bacteria, or fungus or virus. And when it recognizes that target, it's called into duty to clear it from the body. Taking artificial receptors- CAR that can go on to these cells and allow them to recognize what we want them to recognize," he noted. "In this case that's HIV."

First, the team genetically engineered CAR to find and bind to simian/human immunodeficiency virus (SHIV), a lab-engineered HIV hybrid composed of human virus and monkey virus. Then the researchers modified the DNA of certain blood-forming stem cells so they would carry SHIV-killing CAR. The resulting cells were introduced into the bloodstream of four male juvenile SHIV-infected macaque monkeys.

The engineered cells successfully took up residence in each monkey's bone marrow. The cells moved widely throughout the body, targeting and killing SHIV-infected cells, without producing any notable adverse side effects. The advantage of the stem cell-based approach is that once these cells are grafted into the body, they continuously produce new T-cells that have this gene in them that can target HIV cells.

Plans are underway for a human trial, this study shows both that these cells will respond to HIV and that it's safe. This strategy is unlikely to fully work on its own, CAR will most likely need to be used with antiretroviral therapy. CAR therapy is already leading to impressive results in cancer and holds promise for HIV eradication.
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Reovirus could treat brain tumours

A virus injected directly into the bloodstream could be used to treat people with aggressive brain tumours, Scientists have found that the naturally occurring virus could act as an effective immunotherapy in patients with brain cancer or other cancers that have spread to the brain. They showed that a type of virus called reovirus could cross the blood-brain barrier to reach tumours, where it replicates and kills the cancer cells.

They also found that the virus was able to 'switch-on' the body's own defense systems to attack the cancer. The study authors, from the University of Leeds and The Institute of Cancer Research in London, believe reovirus therapy could be used in conjunction with other cancer therapies to make them more potent - and a clinical trial is currently underway. Because the virus infects cancer cells and leaves healthy cells alone, patients receiving the treatment reported only mild flu-like side effects.

Scientists thought it was unlikely that the virus would be able to pass from the blood into the brain because of the blood-brain barrier, a protective membrane around the brain. That would have meant that the only way they could get the virus into the brain was to inject it directly into the brain - which is challenging, would not be suitable for all patients, and cannot be regularly repeated. But the research demonstrated that the virus could be administered through a single-dose intravenous drip.

Nine patients took part in the study, they had cancers that had either spread to the brain from other parts of the body or were fast-growing gliomas, a type of brain cancer that is difficult to treat, and has a poor prognosis. All the patients were due to have the tumours removed surgically. But in the days before the surgeons operated, the patients were given the virus drip.

Once the tumours were removed, samples were taken and analysed for signs that the virus had been able to reach the cancer, sometimes deep within the brain. In all nine patients, there was evidence that the virus had reached its target. The researchers also found that the presence of reovirus stimulated the body's own immune system, with white blood cells or 'killer' T-cells being attracted to the tumour site to attack the cancer.

Tissue samples from patients who had surgery but not the virus therapy served as a control. When compared with the control samples, the tissue taken from the people who had received the reovirus had higher levels of interferons, proteins that 'switch-on' the body's immune system. According to Dr Adel Samson, co-lead author and medical oncologist at the Leeds Institute of Cancer and Pathology, at the University of Leeds, "This is the first time it has been shown that a therapeutic virus is able to pass through the brain-blood barrier, and that opens up the possibility this type of immunotherapy could be used to treat more people with aggressive brain cancers.

Human immune systems aren't very good at detecting cancers, because cancer cells look like human body's own cells, and partly because cancers are good at telling immune cells to turn a blind eye. But the immune system is very good at seeing viruses. In the study, they were able to show that reovirus could infect cancer cells in the brain. And, importantly, brain tumours infected with reovirus became much more visible to the immune system.

Although the earlier trial demonstrated that the reovirus was reaching the cancer cells after just a single dose, doctors have decided to give it repeatedly to patients because of the way it 'kick starts' the body's own defences. The presence of cancer in the brain dampens the body's own immune  system. The presence of the reovirus counteracts this and stimulates the defence system into action. Additional effect of the virus on enhancing the body's immune response to the tumour will increase the amount of tumour cells that are killed by the standard treatment, radiotherapy and chemotherapy.
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Aging impairs immune response to flu

Aging impairs the immune system's response to the flu virus in multiple ways, weakening resistance in older adults, researchers examined the innate immune response to the flu virus. They collected blood samples from healthy young adults and older adults.

They isolated monocytes, a type of white blood cell, from the samples and stimulated the monocytes with either flu virus or a mimic of the virus. The immune response in cells from older adults was severely impaired in critical ways, the researchers found.

To fight the flu virus, the body needs to activate potent antiviral proteins called interferons. But in older adults, this response is weakened by age-related damage to a molecule, TRAF3, that signals immune cells to make interferon. Without that signal, and another involving antiviral genes, resistance to flu falls short.
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Heplisav-B for prevention of Hepatitis B

U.S. Food and Drug Administration (FDA) has approved Heplisav-B [Hepatitis B Vaccine, Recombinant (Adjuvanted)] for prevention of infection caused by all known subtypes of hepatitis B virus in adults. Hepatitis B is an extremely infectious and potentially deadly virus.

 There is no cure for hepatitis B, and infections are on the rise. Hepatitis B can be prevented through effective vaccination. Current hepatitis B vaccines require three shots over a six-month period, however, almost half of adults fail to complete the series within one year.

Prevention of hepatitis B in adults through vaccination is more important than ever given the increase in the rate of infections. A two-dose schedule with higher rates of protection, along with other strategies, may help us move closer to the goal of eliminating hepatitis B.

Hepatitis B is a viral disease of the liver that can become chronic and lead to cirrhosis, liver cancer and death. The hepatitis B virus is 50 to 100 times more infectious than HIV, transmission is on the rise. There is no cure for hepatitis B, but effective vaccination can prevent the disease. In adults, hepatitis B is spread through contact with infected blood and through unprotected sex with an infected person.

 The CDC recommends vaccination for those at high risk for infection due to their jobs, lifestyle, living situations and travel to certain areas. People with diabetes are particularly vulnerable to infection, the CDC recommends vaccination for adults age 19 to 59 with diabetes as soon as possible after their diagnosis, and for people age 60 and older with diabetes.

Heplisav-B is an adult hepatitis B vaccine that combines hepatitis B surface antigen with Dynavax's proprietary Toll-like Receptor (TLR) 9 agonist to enhance the immune response. Dynavax has worldwide commercial rights to Heplisav-B. Heplisav-B is indicated for active immunization against infection caused by all known subtypes of hepatitis B virus. Heplisav-B is approved for use in adults 18 years of age and older.

Do not administer Heplisav-B to individuals with a history of severe allergic reaction like anaphylaxis after a previous dose of any hepatitis B vaccine or to any component of Heplisav-B, including yeast. Appropriate medical treatment and supervision must be available to manage possible anaphylactic reactions following administration of Heplisav-B.

Immunocompromised persons, including individuals receiving immunosuppressant therapy, may have a diminished immune response to Heplisav-B. Hepatitis B has a long incubation period. Heplisav-B may not prevent hepatitis B infection in individuals who have an unrecognized hepatitis B infection at the time of vaccine administration. The most common patient reported adverse reactions reported within 7 days of vaccination were injection site pain, fatigue and headache.
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New way of treating HIV

 HIV drugs target the virus, the virus is not stable; it always mutates because the virus can become resistant to effective drugs, directing the immune system to kill the disease is better than targeting the virus with drug.

Some people are okay with HIV suppressing treatment, but more people are experiencing drug resistance. HIV- 1 is the most widespread, HIV can be classified into R5 and X4 viruses.

R5 viruses are linked with primary infection while X4 viruses occur in later stages of HIV diseases in some HIV patients. Detection of X4 is an indication that the patient's HIV infection has progressed to dangerous state.

Immune system protein suppresses damaging HIV strains, X4, by preventing the virus from infecting cells can be improve on, strengthening the immune system to kill the virus will be more effective because viruses cannot escape the body's immune system.
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Cancer treatment can leads to HIV cure

Cancerous cells and HIV virus multiply in a similar way, both express the same molecules.Certain cancer therapies, like checkpoint inhibitors, could successfully treat HIV.

HIV and cancer patients need strong immune systems to fight diseases; strong immune system can reduce spread of tumours in cancer patients and subdued deadly virus in HIV patients.

Cancer treatment could clear HIV virus, by activating HIV that lies dormant in the patients' cells, because the present HIV drug is unable to detect and kill hidden virus.

Checkpoint inhibitors support the immune system in its fight against cancer, this kind of drug may also activate HIV that lies dormant in cells, and strengthen the immune system to kill the virus.
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Malaria drug protects fetuses from Zika

Zika virus infection can cause brain damage and sometimes death of fetus in the womb, it infects the fetus by manipulating the normal barrier to infection in the body.

Exposure to zika virus activated genes related to autophagy, the virus multiply in the placenta, autophagy process in the placenta promotes zika's survival and it infects the placental cells.

The malaria drug, Hydroxychloroquine suppresses the autophagy response, this reduces the virus in the fetuses and placentas.
With this suppression, their is less damage and the fetuses grow normally.

The malaria drug protects the fetus from the zika virus even when the virus is still present in the mother. It effectively blocks viral transmission to the fetus by interfering with the process of zika virus infection transmission and protects fetus from viral infection.

Hydroxychloroquine suppresses the autophagy response, this reduces the virus in the fetuses and placentas.
With this suppression their is less damage and the fetuses grow normally.
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Zika RNA found in Aedes albopictus

Chelsea Smartt, an entomology associate professor and her research team collected 20 female and 19 male Aede albopictus mosquitoes eggs and raised them to adults and tested the adults for the Zika virus RNA

They discovered that five of them are positive for Zika RNA, this shows that Zika virus is present in mosquito that is not associated with the virus.

Mosquitoes like Aedes albopictus can be infected with zika virus in an area that has high density of zika virus.

Avoid mosquito bites and sleep under insecticide mosquito net at night. Presently, their is no vaccine for zika virus.

New HIV reservoir discovered by scientists

Scientists have discovered a new cell in human body where HIV persists in spite of treatment.

Researchers have tried to clear HIV virus from the white blood cells that is part of immune system.

The virus persists in macrophages of infected person, this shows that T cells and some other cells in the body can serve as reservoir for HIV.

Macrophages are large white blood cell in tissue and bloodstream, the discovery shows that macrophages can be infected and they respond to antiretroviral therapy.

Scientists discovered that macrophages can survive in the body and continue to attack the HIV positive patients when their is therapy interruption.

Victor Garcia, a professor of medicine, microbiology and immunology and his team are trying to find out how HIV continues in tissue macrophages during HIV treatment and how it respond to treatment.

New methods make cells resistant to HIV

Scientists at Scripps Research Institute have discovered a way to tie HIV-fighting antibodies to immune cells, producing a cell population resistant to the virus.

The latest experiment shows that resistance cells can replace disease cells quickly and curing the disease in HIV positive patients.

The new TSRI method is better than therapies where the antibodies float freely in the bloodstream at low concentration.

Antibodies in the new method hang on to a cell's surface, preventing HIV from entering cell receptor and spreading infection.

Scientists used rhinovirus as a model, they used lentivirus to deliver a new gene to cultured human cells.

The gene directed cells to produce antibodies that joined with the human cell receptor ICAM-1 that rhinovirus needs, this prevent virus from entering the cell to spread infection.

Researchers tested the same method against HIV. Strains of HIV joined with a cell surface receptor-CD4 on the immune cell that HIV normally kill.

Scientists confirmed that the antibodies prevent HIV in a better way than free-floating, HIV is treatable but not curable.

Another type of mosquito may transmit Zika virus

The main carrier of Zika is yellow fever mosquito, researchers have found traces of zika virus in Asian tiger mosquitoes collected in Brazil.

According to Chelsea Smartt, their is no proof that Asian tiger mosquitoes can transmit zika but their is need for more research to detect other carriers of zika.

Smartt and her colleagues hatched mosquitoes egg in Brazil and discovered that Asian tiger males tested positive to Zika RNA but negative to the live Zika virus test.

She suggested zika virus test for all the mosquitoes in the area with a higher number of Zika cases for Zika RNA, if the mosquitoes are positive to Zika RNA they need to undergo live Zika virus test.

Previous exposure to flaviviruses can enhance effects of Zika

Flavivirus is a group of related viruses, some of them are West Nile virus, dengue virus, yellow fever virus, Zika virus and others.

A new study that used human samples tested in mice discovered that prior infection with any flavivirus can increase the chance of Zika infection.

Exposure to one of these virus leads to more disease when exposed to related virus. Zika is spreading very fast in regions that is prone to other flaviviruses.

Human antibodies were transferred from infected human to mice to expose them to Zika virus.

The mice not giving antibodies survived Zika infection while those that received infected human antibodies did not.

Effects of Zika virus on your heart

Zika virus is primarily transmitted  through the bite of an infected Aedes mosquitoes. Centers for Disease Control and Prevention (CDC) has confirmed that Zika can spread through sex, infected blood during transfusion and pregnant mother to foetus.

This virus could harm the heart by damaging the  heart muscle cells or by promoting inflammation in the heart of infected people, Zika is also linked to autoimmune disorder that causes muscle weakness and paralysis.

People infected with zika virus should get enough rest, drink enough water and seek medical care, presently there is no vaccine available for zika virus.

Zika can be prevented by wearing light- coloured clothes that cover every parts of the body and sleeping inside insecticide treated mosquito net.