Impact of global warming on viral diseases: what is the evidence?

Global warming is believed to induce a gradual climate change. Hence, it was predicted that tropical insects might expand their habitats thereby transmitting pathogens to humans. Although this concept is a conclusive presumption, clear evidence is still lacking--at least for viral diseases. Epidemiological data indicate that seasonality of many diseases is further influenced by strong single weather events, interannual climate phenomena, and anthropogenic factors. So far, emergence of new diseases was unlinked to global warming. Re-emergence and dispersion of diseases was correlated with translocation of pathogen-infected vectors or hosts. Coupled ocean/atmosphere circulations and 'global change' that also includes shifting of demographic, social, and economical conditions are important drivers of viral disease variability whereas global warming at best contributes.     

Phosphoinositides: older than we first thought?

Despite nearly 50 years of study, it is good to see that phosphoinositides are still capable of springing the odd surprise. Signaling by the second messenger phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P(3)) was thought to be absent in yeast, but a recent paper now describes the presence of PtdIns(3,4,5)P(3) in Schizosaccharomyces pombe.     

Adult leukaemia: what is the role of currently known risk factors?

Leukaemias are a heterogeneous group of tumours including acute and chronic forms. Considerable efforts have been made to identify risk factors for these diseases, but only a minority of leukaemia cases can currently be attributed to identified or hypothesized factors. This review highlights recent epidemiological literature concerning adult leukaemia, discussing in detail the hereditary, environmental and medical risks. Chromosomal syndromes and genetically based diseases carry a high risk of leukaemia, but rarely occur in the population. Environmental and occupational exposures to chemicals including pesticides have been widely studied, although the results are not consistent, with the exception of benzene. Smoking seems to be a weak causal risk factor. The risk of ionizing radiation has further been quantified in recent studies, although the effects of low doses have not yet been clarified. The results for non-ionizing radiation continue to be inconsistent, but a large effect of electromagnetic fields on the risk of leukaemia appears to be unlikely. Medically applied radio- and chemotherapy are clearly associated with subsequent leukaemia development, and there are links between leukaemia and viral infections. Future research should emphasize the shortcomings in exposure assessment that pervade many studies, and interactions between different risk factors need to be taken into consideration. Received: 25 September 1997 / Accepted in revised form: 14 October 1997     

What is the risk of a deadly adenovirus pandemic?

Many of us had refresher courses in virology, immunology, and epidemiology in 2020, and we were reminded of the fact that Homo sapiens, the wiliest predator on the planet, has been hunting everything that moves for millennia. These repeated interspecies contacts inherently lead to recurrent zoonosis (nonhuman to human) and anthroponosis (human to nonhuman). Given the accelerating changes in our ecosystems since the neolithic revolution, it was not surprising to see a virus that spreads via aerosolization and liquid droplets cause a pandemic in a few months. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) pandemic begs the question—which viruses could cause a global threat? In this Opinion, the characteristics that make adenoviruses a risk, which include efficient intra- and interspecies transmission, thermostable particles, persistent/latent infections in diverse hosts, and the ability to readily recombine and escape herd immunity, are discussed.     

What is the role of autophagy in HIV-1 infection?

HIV-1 infection is characterized by a progressive CD4 T cell depletion. It is now accepted that apoptosis of uninfected bystander CD4 T lymphocytes plays a major role in AIDS development. Viral envelope glycoproteins (Env) are mainly involved in inducing this cell death process, but the mechanisms triggered by HIV-1 leading to immunodeficiency are still poorly understood. Recently, we have demonstrated that autophagy is a prerequisite for Env-mediated apoptosis in uninfected CD4 T cells, underlining its role in HIV-1 infection. However, occurrence of autophagy in HIV-1-infected cells has not yet been described. Several hypotheses are discussed, based on the comparison with data from other viral infections.     

Xenografts: are the risks so great that we should not proceed?

Animal organs could save patients needing transplants, but further research is necessary to resolve remaining problems with organ rejection. Furthermore, xenotransplantation risks transmitting animal pathogens to patients and to the general population. It would be unethical to proceed with clinical trials before principles and procedures for dealing with this risk are in place.     

What is the role of autophagy in HIV-1 infection?

HIV-1 infection is characterized by a progressive CD4 T cell depletion. It is now accepted that apoptosis of uninfected bystander CD4 T lymphocytes plays a major role in AIDS development. Viral envelope glycoproteins (Env) are mainly involved in inducing this cell death process, but the mechanisms triggered by HIV-1 leading to immunodeficiency are still poorly understood. Recently, we have demonstrated that autophagy is a prerequisite for Env-mediated apoptosis in uninfected CD4 T cells, underlining its role in HIV-1 infection. However, occurrence of autophagy in HIV-1-infected cells has not yet been described. Several hypotheses are discussed, based on the comparison with data from other viral infections.     

Xenotransplantation: from animal facility to the clinic?

Since 1960, clinical organ transplantation has evolved from an experimental procedure to highly successful ‘routine’, but as technical advances have extended eligibility to more victims of end-stage organ disease, the supply of donor organs has lagged behind. Urgency of need, probability of success and ability to pay are often used to limit waiting lists; without these, as many as 124 000 transplants per year could be performed in the USA alone. Although the supply of organs from human donors may well be assisted in future by increased public education and changes in donor laws, it is unlikely that the need for organs will ever be met by generosity and calamity alone — hence the enthusiasm for other sources of organs.     

Can we really predict risk of cancer?

Background: Growing awareness of the potential to predict a person's future risk of cancer has resulted in the development of numerous algorithms. Such algorithms aim to improve the ability of policy makers, doctors and patients to make rational decisions about behaviour modification or surveillance, with the expectation that this activity will lead to overall benefit. There remains debate however, about whether accurate risk prediction is achievable for most cancers. Methods: We conducted a brief narrative review of the literature regarding the history and challenges of risk prediction, highlighting our own recent experiences in developing tools for oesophageal adenocarcinoma. Results and conclusions: While tools for predicting future risk of cardiovascular outcomes have been translated successfully to clinical practice, the experience with cancer risk prediction has been mixed. Models have now been developed and validated for predicting risk of melanoma and cancers of the breast, colo-rectum, lung, liver, oesophagus and prostate, and while several of these have adequate performance at the population-level, none to date have adequate discrimination for predicting risk in individual patients. Challenges of individual risk prediction for cancer are many, and include long latency, multiple risk factors of mostly small effect, and incomplete knowledge of the causal pathways.     

Toxoplasma gondii infection: What is the real situation?

The prevalence of chronic Toxoplasma infections reported in the literature varies enormously. We hypothesize that one factor could be due to the different methods used in the evaluation of infections. Serological evidence of Toxoplasma infections in 450 pregnant women (PW) and 300 HIV-infected patients (HIV) were investigated by the Sabin–Feldman dye test and two other commercial ELISA kits (kit1 and kit2). Anti-Toxoplasma IgG antibodies obtained from the Sabin–Feldman dye test, ELISA kit1 and ELISA kit2 in the PW subjects were 14.7%, 29.6% and 38.7%, and in the HIV subjects were 13%, 34.7% and 36.3%, respectively. So there were significant differences in the seroprevalences when different diagnostic tests were used (P < 0.05). Regarding Sabin–Feldman dye test as the gold standard for anti-Toxoplasma antibodies detection, we found that the sensitivity and specificity of the ELISA kit1 and kit2 was in the range of their specification. However as the two ELISA kits used in our study identified a much higher prevalence of Toxoplasma infections which indicated that false positive cases were being reported. Based on results obtained, it is therefore highly recommended that research workers should be aware that the reports of serological studies in terms of high positive results should be treated with some skepticism until additional precise diagnostic tools are developed.     

Alcodemia: are we training our students to be great thinkers or great drinkers?

Academia has fostered an unhealthy relationship with alcohol that has an undeniable impact on the health and behaviour of students and staff. Subject Categories: S&S: History & Philosophy of Science, Chemical Biology, S&S: Ethics

University life has a lot to offer. And, for better or worse, much of it goes hand in hand with a bottle. Believe it or not, I was a bit of teetotaler in my undergraduate days but quickly made up for it in graduate school, where each celebration included inebriation. Indeed, my initial tour of the laboratory I eventually worked in included a refreshing visit to the grad club. Orientation week ended with a marathon beer blitz at a nightclub. The semester’s first invited seminar speaker was welcomed with the sounds of loose change, ice buckets and the clickity‐clack of organic microbrews being opened. Our inaugural genome evolution journal club was such a success that we vowed to spill even more red wine onto our notebooks the following week. In hindsight, I should have realized at this early stage in my studies that I was fostering an unhealthy and unsustainable relationship between biology and booze. Unfortunately, my post‐graduate education in alcohol didn’t stop there.Like many keen students, I arrived at my first scientific conference with a belly full of nerves and a fistful of drink tickets, which I quickly put to good use at the poster session. The successful completion of my PhD proposal assessment was met with pats on the back as I was swiftly marched off to a local pub with no chance of escape. My first peer‐reviewed paper literally arrived with a pop as Champagne was generously poured into plastic cups for the entire laboratory group. My failures, too, were greeted with a liberal dose of ethanol. “Sorry you came up short on that scholarship application, Smitty. It’s nothing a little weapons‐grade Chianti won’t cure.” “That experiment failed again! Come on, let me buy you a lunchtime martini to make up for it.” Soon I learnt that every academic event, achievement or ailment, no matter how big or small, could be appropriately paired with beer, wine or spirit. Missing from the menu were two crucial ingredients for any burgeoning researcher: moderation and mindfulness.But it was the older vintages that really inspired me – the legendary drinking escapades of my scientific mentors, advisors and idols. The tale of professor so‐and‐so who at that epic meeting in 1993 polished off an entire magnum of rosé at dinner and then went on to deliver among the greatest keynote lectures on record at 9 am the following morning. That celebrated chaired researcher who kept the single malt next to the pipette tips for quick and easy access. The grizzled evolutionary ecologist who never went into the field without half a dozen cans of high‐end smoked oysters and two hip flaks, which didn’t contain water. And so, when I was told by someone in the know of how the most famous geneticist on campus wrote that monumental Nature paper (the one I’d read ten times!) while locked in his office for twelve hours with a six‐pack, I bought into the romance hook, line and sinker. The result: I’ve been nursing a recurring headache for nearly two decades and I’m still waiting on that Nature paper. Most importantly, I now realize the various dangers of romanticizing the bottle, especially for individuals in mentorship positions.Like my idols before me, I’ve accrued a cask full of well‐oaked academic drinking stories, except that they haven’t aged well. There is that heroic evening of intense scotch‐fueled scientific discussion, which led to me forfeiting two front teeth to the concrete sidewalk (my mother still thinks it was a squash accident). Or that time I commemorated the end of a great conference in Barcelona by throwing up on the front window of a café while the most prominent minds in my field sipped aperitifs inside (thank god this was before Twitter). Even more romantic: me buying a bottle of Cotes de Nuits Burgundy at Calgary airport on route to a job interview, discreetly opening the bottle in‐flight because economy class wine sucks, and then being met by airport security upon landing. Let’s just say I didn’t get the job. To some, these anecdotes might seem light‐hearted or silly, but they are actually rather sad and underscore the seriousness of substance abuse. Many readers will have their own complicated experiences with alcohol in academia and, I believe, will agree that it is high time we asked ourselves: are we training our graduate students to be great thinkers or great drinkers? Moreover, this question does not address the equally if not more serious issue of excessive drinking among undergraduate students.As I sit at my desk writing this, I think to myself: is it normal that within a two‐minute walk of my university office there are three different places on campus that I can have a beer before lunch, not including the minifridge behind my desk? Is it normal that in my department the first thing we do after a student defends their thesis is go to the grad club where they can have any alcoholic drink of their choosing for free from the goblet of knowledge, which is kept on a pedestal behind the bar? Is it normal that before the COVID pandemic when I was visiting a prominent university for an invited talk, one of the professors I met with offered me a glass of expensive Japanese gin at 11 am in the morning? (And, yes, I accepted the drink.)Of course, if you don’t want to drink you can just say no. But we are learning more and more how institutional cultures – “the deeply embedded patterns of organisational behaviour and the shared values, assumptions, beliefs or ideologies that members have about their organisation or its work” (Peterson & Spencer, 1991) – can have powerful effects on behaviour. Excessive alcohol consumption is undeniably an aspect of collegial culture, one that is having major impacts on the health and behaviour of students and staff, and one that I’ve been an active participant in for far too long. I’ll be turning forty in a few months and I have to face the fact that I’ve already drunk enough alcohol for two lifetimes, and not one drop of it has made me a better scientist, teacher or mentor. The question remains: how much more juice can I squeeze into this forty‐year‐old pickled lemon? Well, cheers to that.     

Xenotransplantation: hope or delusion?

Having moved from the realms of science fiction to a rapidly growing research area, xenotransplantation promises numerous benefits to patients in the future. However, deep suspicions of this technology are rife. We suggest an alternative viewpoint to that given in E M Engels' article in Biologist 46(2).     

Lipid rafts as viral entry routes and immune platforms: A double-edged sword in SARS-CoV-2 infection?

Lipid rafts are nanoscopic compartments of cell membranes that serve a variety of biological functions. They play a crucial role in viral infections, as enveloped viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can exploit rafts to enter or quit target cells. On the other hand, lipid rafts contribute to the formation of immune synapses and their proper functioning is a prerequisite for adequate immune response and viral clearance. In this narrative review we dissect the panorama focusing on this singular aspect of cell biology in the context of SARS-CoV-2 infection and therapy. A lipid raft-mediated mechanism can be hypothesized for many drugs recommended or considered for the treatment of SARS-CoV-2 infection, such as glucocorticoids, antimalarials, immunosuppressants and antiviral agents. Furthermore, the additional use of lipid-lowering agents, like statins, may affect the lipid composition of membrane rafts and thus influence the processes occurring in these compartments. The combination of drugs acting on lipid rafts may be successful in the treatment of more severe forms of the disease and should be reserved for further investigation.