Lifeboat Foundation

Norovirus, a highly infectious virus that is the leading cause of diarrhea and vomiting in the U.S., has no approved therapeutics or vaccines to prevent its miserable effects. This is partly due to a lack of reliable animal models to study norovirus infection and predict how effective interventions would be in people. To solve this, NIAID scientists have developed an animal model to study human norovirus infection that could help facilitate the development of new vaccines and therapeutics to treat norovirus infection. Findings from this research were published Feb. 6 in Nature Microbiology.

Human norovirus causes illness in tens of millions of people in the U.S. each year and, in some cases, can result in hospitalization and even death. It is easily spread when people ingest foods, drinks or particles from surfaces contaminated by virus from the stool or vomit of an infected individual. Noroviruses are genetically diverse, with different genogroups—groups characterized by genetic similarity—of the virus infecting different species of animals. Several genogroups of noroviruses infect people without similarly infecting animals. This has led to difficulties in establishing an animal model for human norovirus infection.

Following up on earlier evidence that rhesus macaque monkeys could develop norovirus infections, a team of researchers led by scientists at NIAID’s Vaccine Research Center set out to determine whether macaques could serve as an effective animal model for the human disease. The macaques were challenged with several genotypes of human noroviruses at once. Throughout the experiment, the animals were kept in biocontainment, and their health and behavior were carefully monitored. Levels of virus in the animals’ stool were measured, and antibodies against norovirus in the animals’ blood serum were analyzed. The researchers found that the macaques were susceptible to viral infection with at least two genotypes of norovirus, with similar antibody responses, shedding of virus in stool, and pathology as in human norovirus infection. Notably, the infections in the animals did not result in clinical symptoms, such as diarrhea and vomiting.

A new test invented by University of Illinois Chicago researchers allows dentists to screen for the most common form of oral cancer with a simple and familiar tool: the brush.

The diagnostic kit, created and patented by Guy Adami and Dr. Joel Schwartz of the UIC College of Dentistry, uses a small brush to collect cells from potentially cancerous lesions inside the mouth. The sample is then analyzed for genetic signals of oral squamous cell carcinoma, the ninth most prevalent cancer globally.

This new screening method, which is currently seeking commercialization partnerships, improves upon the current diagnostic standard of surgical biopsies-an extra referral step that risks losing patients who sometimes don’t return until the cancer progresses to more advanced, hard-to-treat stages.

Women are more likely than men to have conditions such as lupus, rheumatoid arthritis, and autoimmune hepatitis (depicted above in a cellular micrograph), in which their immune response attacks healthy, functioning parts of their body. Yet the reason behind this sex-based imbalance has long eluded scientists. Now, a study published last week in proposes that a molecule associated with the X chromosome may be partly to blame. Researchers noticed that many of the proteins commonly targeted by the immune system in people with autoimmune diseases had something in common: They help a molecule called Xist carry out its function. Xist molecules act a bit like quality control inspectors for women’s extra X chromosomes, preventing them from producing a toxic amount of proteins. The scientists suspect that when immune cells encounter large bunches of these Xist-related proteins—for instance, when a dead cell spills them into the bloodstream—they may react by making antibodies to attack them throughout the body. To test the idea, the team studied genetically engineered mice in which both males and females produced Xist. Like their female counterparts, these males were also at an increased risk of developing severe cases of lupus. The researchers also found that people with autoimmune disorders had more antibodies for Xist-related proteins in their blood. Still, Xist molecules may not be the only factor at play: Experts note that some people produce these Xist-related antibodies without developing autoimmune disorders, reports.

Ball is not alone in calling for a drastic rethink of how scientists discuss biology. There has been a flurry of publications in this vein in the past year, written by me and others^2–4. All outline reasons to redefine what genes do. All highlight the physiological processes by which organisms control their genomes. And all argue that agency and purpose are definitive characteristics of life that have been overlooked in conventional, gene-centric views of biology.

This burst of activity represents a frustrated thought that “it is time to become impatient with the old view”, as Ball says. Genetics alone cannot help us to understand and treat many of the diseases that cause the biggest health-care burdens, such as schizophrenia, cardiovascular diseases and cancer. These conditions are physiological at their core, the author points out — despite having genetic components, they are nonetheless caused by cellular processes going awry. Those holistic processes are what we must understand, if we are to find cures.

Ultimately, Ball concludes that “we are at the beginning of a profound rethinking of how life works”. In my view, beginning is the key word here. Scientists must take care not to substitute an old set of dogmas with a new one. It’s time to stop pretending that, give or take a few bits and pieces, we know how life works. Instead, we must let our ideas evolve as more discoveries are made in the coming decades. Sitting in uncertainty, while working to make those discoveries, will be biology’s great task for the twenty-first century.

Using a new technique, scientists created genetic blueprints for kangaroos, penguins, sharks and more.

Some hereditary genetic defects cause an exaggerated immune response that can be fatal. Using the CRISPR-Cas9 gene-editing tool, such defects can be corrected, thus normalizing the immune response, as researchers led by Klaus Rajewsky from the Max Delbrück Center now report in Science Immunology.

Familial hemophagocytic lymphohistiocytosis (FHL) is a rare disease of the immune system that usually occurs in infants and young children under the age of 18 months. The condition is severe and has a high mortality rate. It is caused by various gene mutations that prevent cytotoxic T cells from functioning normally. These are a group of immune cells that kill virus–infected cells or otherwise altered cells.

If a child with FHL contracts a virus—such as the Epstein-Barr virus (EBV), but also other viruses—the cytotoxic T cells cannot eliminate the infected cells. Instead, the immune response gets out of control. This leads to a cytokine storm and an excessive inflammatory reaction that affects the entire organism.

Plant cell-surface receptors that are known to participate in immunity, development, and reproductive processes include the LRR-, G-lectin-, Wall-associated kinase (WAK)-, Domain of Unknown Function 26 (Duf26)-, L-lectin-, Lysin motif (LysM)-, and Malectin-containing RLKs and RLPs (Fig. 1a–h). There are additional RLK families with different ectodomains, such as the proline-rich extensin-like receptor kinases (PERKs) and thaumatin-like protein kinases (TLPKs)^9,13. However, their function in immunity is not well-characterized. Cell-surface receptors with LRR-, G-lectin-, WAK-, and LysM-ectodomains have been reported to recognise PAMPs, while others perceive self-molecules or unidentified ligands (Fig. 1h; Supplementary Fig. 1). Recognition of the diverse array of ligands is likely to be accomplished by variable structures and combinations of different ectodomains (Fig. 1a–g). To trace the origins of different receptor classes within the plant lineage, we first identified RLKs and RLPs in 350 genomes from Glaucophyta, red algae, green algae, Bryophytes, and Tracheophytes. We define here RLKs as any proteins with both 1–2 TMs and KDs, and RLPs as any protein with 1–2 TMs, but lack KDs. In total, we identified 177,645 RLKs, almost up to 70% of which possess either LRR-, G-lectin-, WAK-, Duf26-, L-lectin-, LysM-and Malectin-ectodomains (Fig. 1i). Next, we searched for proteins with these ectodomains and TMs that lack KDs and found 41,144 RLPs (Fig. 1j). We further examined which of the identified RLKs and RLPs families are likely to be involved in immunity. A previous report suggested a positive correlation between the gene family sizes of cell-surface immune receptors and intracellular immune receptors (the NB-ARC family) across the angiosperms⁴. We examined the correlation between the relative size (%; number of identified genes in the family/numbers of searched genes × 100; see methods) of the RLK families, the RLPs families, and the NB-ARC family in each genome. Notably, most RLK families (except for the LysM-RLKs) exhibit positive correlations with the NB-ARC family, while most RLP families (except for the LRR-RLPs) do not exhibit positive correlation with the NB-ARC family (Main Fig. 1k). Furthermore, we checked the expression level of these receptor families in Arabidopsis thaliana during immunity. Notably, the RLKs, except for LRR-and Malectin-RLKs, generally exhibit higher expression levels compared to the RLPs during immunity (Main Fig. 1k; Supplementary Fig. 2). These data collectively suggest that the RLKs are more likely to be involved in immunity than the RLPs.

Next, we examined the presence or absence of ectodomains (LRR-, G-lectin-, WAK-, Duf26-, L-lectin-, LysM-and Malectin-ectodomains lacking TM or KD; ectodomain-only proteins), RLPs (TM-bound ectodomains) and RLKs (ectodomains encompassing both TM and KD) in the plant lineage (Fig. 2; Supplementary Fig. 3; Supplementary Data 1a–c). Ectodomains exhibit an ancient heritage, with LRR-, WAK-, LysM-, Malectin-, and L-lectin-domains dating back to the era of Glaucophyta. Similarly, relatively ancient counterparts such as LRR-RLPs, WAK-RLPs, LysM-RLPs, Malectin-RLPs, and L-lectin-RLPs are found in both Glaucophyta and Rhodophyta. In contrast, RLKs emerged more recently. Green algae harbour WAK-RLKs, Malectin-RLKs, and G-lectin-RLKs, and LysM-RLKs, L-lectin-RLKs, and Duf-26-RLKs are exclusive to Embryophytes (Fig. 2). Except for LRR-RLPs, all six families of RLP are basal to the RLK families.

Colorectal cancer (also called bowel cancer) typically develops in the large bowel (colon) or rectum. Recent studies have shown significant rises in the number of colorectal cancer cases, particularly those in young adults. As we discussed earlier, the recently released estimated cancer statistics for 2024 predict colorectal cancer as the leading cause of mortality in men under 50 and the second-leading cause of mortality in women. Additionally, experts predict over 150,000 new cases of colorectal cancers this year.

To combat these troubling figures, ongoing research focused on the prevention and treatment of colorectal cancers remains a high priority and urgent need. This includes data recently published in Science Advances which demonstrates pre-clinical efficacy for a new treatment approach.

The study involves genetic material known as microbial or mislocalized DNA. This type of DNA arrises from cells that become damaged, thus no longer providing the correct genetic instructions. Damaged DNA can elicit various reactions in the body, including activating the immune response. Damaged DNA can therefore influence how the body responds to diseases, including colorectal cancer.

Scientists from the German Cancer Research Center (DKFZ) and Heidelberg University have investigated in mice how spreading tumor cells behave at the site of metastasis. Some tumor cells immediately start to form metastases. Others leave the blood vessel and may then enter a long period of dormancy. What determines which path the cancer cells take is their epigenetic status. This was also confirmed in experiments with human tumor cells. The results of the study could pave the way for novel diagnostic and therapeutic applications.

The work appears in Nature Cancer.

What makes cancer so dangerous? Cancer cells that leave the primary tumor to reach distant sites of the body where they may grow into daughter tumors, called metastases. While most primary tumors can be effectively treated, metastases are the real danger. Oncologists estimate that more than 90% of all cancer deaths in solid tumors are due to metastases.