Interactions between flu subtypes predict epidemic severity more than virus evolution

An analysis of influenza virus evolution over 22 years of flu seasons reveals the major drivers of disease transmission and epidemic severity

Peer-Reviewed Publication

ELIFE

Researchers have shed new light on how viral evolution, population immunity, and the co-circulation of other flu viruses shape seasonal flu epidemics.

The research, published today as a Reviewed Preprint in eLife, explores the relationships among evolutionary and epidemiological quantities in influenza, and presents fundamental findings that substantially advance our understanding of the drivers of influenza epidemics, according to the eLife editors. The authors used a rich set of data sources to provide what the editors say is compelling evidence on the roles of genetic distance, influenza subtype dynamics, and epidemiological indicators in predicting flu epidemics. The findings highlight genetic distance and subtype interference as key factors in determining the timing and severity of annual outbreaks. 

Influenza viruses continually accumulate genetic changes in two key proteins displayed on their surface – called haemagglutinin (HA) and neuraminidase (NA) – a process known as antigenic drift. Antigenic drift allows the virus to escape immune recognition in people who have been vaccinated or had a previous infection, leaving them exposed to re-infection. Of the two types of influenza viruses that routinely circulate together in humans (influenza A and B), influenza A, and particularly subtype A(H3N2), has the fastest rates of antigenic drift and causes the most severe illness and death.

Amanda Perofsky, the lead author of the study and  a research scientist at the Brotman Baty Institute, University of Washington, US, and Fogarty International Center, National Institutes of Health, US, says: “In theory, antigenic drift will lead to more susceptible individuals, which in turn should lead to more flu infections and larger or more severe epidemics. However, prior evidence for this in epidemiological data has been mixed. Mutations in HA are considered to cause the majority of antigenic drift, so surveillance efforts to monitor and predict influenza evolution focus on HA. There has been less focus on NA, even though antibodies against NA also correlate with immunity and influence infection severity. Moreover, outside of flu pandemics, little is known about how different cocirculating influenza subtypes potentially interfere with each other, affecting the size of outbreaks.”

In this study, Perofsky and colleagues from the Fred Hutchinson Cancer Center, the Icahn School of Medicine at Mount Sinai, US Centers for Disease Control and Prevention, and World Health Organization tracked A(H3N2) evolutionary dynamics – measured by both genetic sequences and serological assays – and linked this to epidemiological flu surveillance data in the US over 22 influenza seasons before the COVID-19 pandemic.

They started out by identifying different indicators of flu evolution each season, using HA and NA genetic sequence data from the Global Initiative on Sharing Avian Influenza Data (GISAID) Epiflu database and serological data on immune cross-reactivity between viruses provided by World Health Organization Global Influenza Surveillance and Response System (GISRS) Collaborating Centres in Tokyo, London, Melbourne and Atlanta. They created phylogenetic trees showing lines of evolution of A(H3N2) viruses over time and measured genetic and antigenic distances between viruses circulating in consecutive seasons, to show how far apart the viruses evolved in that timeframe.

Next, the team explored which of these measures of viral ‘fitness’ are most strongly related to variation across A(H3N2) flu outbreaks in different years. When comparing the predictive performance of sequence-based and serological evolutionary metrics, they found that genetic distances based on broad sets of antigenic sites (“epitopes”) in HA and NA had the strongest, most consistent relationship with the disease burden of annual epidemics, rates of virus transmission, and severity of infection, and influenced the dominant subtype of influenza A – A(H3N2) or A(H1N1) – circulating in each season.

When relating genetic distance in HA versus NA to A(H3N2) epidemiology, antigenic drift of H3 (the HA antigen of the A(H3N2) virus) was more strongly linked to epidemic size, viral transmissibility, the age distribution of cases, and the number of excess deaths caused by the A(H3N2) virus, while antigenic drift of N2 (the NA antigen of the A(H3N2) virus) was more strongly linked to the intensity of epidemics (the “sharpness” of the epidemic curve) and greater prevalence of A(H3N2) cases relative to A(H1N1) cases in the population. Increased drift in N2 was also associated with fewer days from epidemic onset to peak incidence (a measure of the speed of the epidemic).

“The direct link between NA antigenic drift and A(H3N2) incidence patterns was a surprising and key result from our study,” says Perofsky. “We expected HA to exhibit stronger associations with seasonal incidence, given that it elicits a stronger immune response than NA.”

Taken together, the authors’ results showed that greater antigenic drift in both HA and NA was linked to larger, more intense epidemics, higher transmission, a greater dominance of the A(H3N2) subtype, and more cases in adults than children. 

Finally, the team applied machine learning models to assess the relative importance of viral evolution, prior population immunity, the co-circulation of other flu viruses, and vaccine coverage and effectiveness in predicting regional A(H3N2) epidemic dynamics. Using one of the models (called a random forest) they could accurately predict regional epidemic size, peak incidence, and subtype dominance patterns of seasonal outbreaks that occurred between 1997 and 2019. Surprisingly, they found that the incidence of A(H1N1) was more predictive of A(H3N2) epidemics than viral evolution, suggesting that interactions between different viral subtypes – that is, subtype interference – play a key role in influenza type A infection dynamics.

“Our study shows that influenza epidemic dynamics are shaped in part by the virus’ antigenic drift in both surface proteins, and that genetic sequence indicators of antigenic drift were more informative than serological (or antibody) data for predicting epidemics in the timeframe analysed,” concludes senior author Cécile Viboud, a staff scientist at Fogarty International Center, National Institutes of Health, US. “Our work is the first to link NA antigenic drift to epidemic burden, timing, and the age distribution of infections. The connection between NA drift and seasonal incidence further highlights the importance of monitoring evolution of both HA and NA to inform the selection of strains for annual flu vaccines and epidemic forecasting efforts.”

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About eLife

eLife transforms research communication to create a future where a diverse, global community of scientists and researchers produces open and trusted results for the benefit of all. Independent, not-for-profit and supported by funders, we improve the way science is practised and shared. In support of our goal, we have launched a new publishing model that ends the accept/reject decision after peer review. Instead, papers invited for review will be published as a Reviewed Preprint that contains public peer reviews and an eLife assessment. We also continue to publish research that was accepted after peer review as part of our traditional process. eLife receives financial support and strategic guidance from the Howard Hughes Medical Institute, Knut and Alice Wallenberg Foundation, the Max Planck Society and Wellcome. Learn more at https://elifesciences.org/about.

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JOURNAL

eLife

DOI

10.7554/eLife.91849.1 

ARTICLE TITLE

Antigenic drift and subtype interference shape A(H3N2) epidemic dynamics in the United States

ARTICLE PUBLICATION DATE

13-Feb-2024

 

New trial highlights incremental progress towards a cure for HIV-1

Peer-Reviewed Publication

UNIVERSITY OF NORTH CAROLINA HEALTH CARE

 

IMAGE: 

CYNTHIA L. GAY, MD, MPH

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CREDIT: UNC DEPARTMENT OF MEDICINE

CHAPEL HILL, N.C. – Antiretroviral therapies (ART) stop HIV replication in its tracks, allowing people with HIV to live relatively normal lives. However, despite these treatments, some HIV still lingers inside cells in a dormant state known as "latency." If ART is discontinued, HIV will awaken from its dormant state, begin to replicate, and cause acquired immunodeficiency syndrome (AIDS). To create a cure, researchers have been attempting to drive HIV out of latency and target it for destruction.

A new clinical trial led by Cynthia Gay, MD, MPH, associate professor of infectious diseases, David Margolis, MD, the Sarah Kenan Distinguished Professor of Medicine, Microbiology & Immunology, and Epidemiology, and other clinicians and researchers at the UNC School of Medicine suggests that a combination of the drug vorinostat and immunotherapy can coax HIV-infected cells out of latency and attack them.

The immunotherapy was provided by a team led by Catherine Bollard, MD, at the George Washington University, who took white blood cells from the study participants and expanded them in the laboratory, augmenting the cells’ ability to attack HIV-infected cells, before re-infusion at UNC.

Their results, published in the Journal of Infectious Diseases, showed a small dent on the latent reservoir, demonstrating that there is more work to be done in the field.

“We did show that this approach can reduce the reservoir, but the reductions were not nearly large enough, and statistically speaking were what we call a “trend” but not highly statistically significant,” said David Margolis, MD, director of the HIV Cure Center and senior author on the paper. “We need to create better approaches to flush out the virus and attack it when it comes out. We need to keep chipping away at the reservoir until there's nothing there.”

DNA inside cell nuclei is kept in a tightly packed space by chromosomes, which act as highly organized storage facilities. When you unfurl a chromosome, you'll find loop-de-loop-like fibers called chromatin. If you keep unfurling, you'll see long strands of DNA wrapped around scaffold proteins known as histones, like beads on a string. Finally, when the unfurling is complete, you will see the iconic DNA double helix.

Vorinostat works by inhibiting a lock-like enzyme called histone deacetylase. By stopping this mechanism, tiny doors within the chromatin fibers unlock and open up, effectively “waking up” latent HIV from its slumber and making it vulnerable to an immune system attack. As a result, a tiny blip of HIV expression shows up on very sensitive molecular assays.

But the effects of vorinostat are short lived, only lasting a day per dose. For this reason, Margolis and other researchers are trying to find safe and effective ways to administer the drug and keep the chromatin channels open for longer periods of time.

For the study, six participants were given multiple doses of vorinostat. Researchers then extracted immune cells from the participants and expanded the cells that knew how to attack HIV-infected cells.

This immunotherapy method, which has been successful against other viruses such as Epstein-Barr virus and cytomegalovirus, involves giving participants back their expanded immune cells in the hopes that these cells will further multiply in number and launch an all-out attack on the newly exposed HIV-infected cells.

However, in the first part of this study, only one of the six participants saw a drop in their HIV reservoir levels. To test whether the result was simply random or something more, researchers gave three participants their usual dose of vorinostat, but introduced five times the amount of engineered immune cells. All three of the participants had a slight decline in their reservoirs.

But, statistically speaking, the results were not large enough to be definitive.

“This is not the result we wanted, but it is research that needed to be done,” said Margolis. “We are working on improving both latency reversal and clearance of infected cells, and we hope to do more studies as soon as we can, using newer and better approaches.”

Many of the participants in the study have been working with Margolis’s research team for years, sacrificing their own time and blood for research efforts. Their long-term partnership and commitment have been essential for data collection. The data, which follows the size of the viral reservoir in these people over years prior to this study, makes the small changes found more compelling.

“People living with HIV come in a couple of times a year, and we measure residual traces of virus in their blood cells, which doesn’t have any immediate benefit to them,” said Margolis. “It’s a very altruistic action and we couldn't make any progress without their help.”

About UNC School of Medicine

The UNC School of Medicine (SOM) is the state’s largest medical school, graduating more than 180 new physicians each year. It is consistently ranked among the top medical schools in the US, including 7th overall for primary care by US News & World Report, and 7th for research among public universities. More than half of the school’s 1,700 faculty members served as principal investigators on active research awards in 2021. Two UNC SOM faculty members have earned Nobel Prize awards.

# # #

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JOURNAL

The Journal of Infectious Diseases

DOI

10.1093/infdis/jiad423 

SUBJECT OF RESEARCH

Not applicable

ARTICLE TITLE

The Effects of Human Immunodeficiency Virus Type 1 (HIV-1) Antigen-Expanded Specific T-Cell Therapy and Vorinostat on Persistent HIV-1 Infection in People With HIV on Antiretroviral Therapy

ARTICLE PUBLICATION DATE

13-Feb-2024

Stopping HIV in its tracks

Peer-Reviewed Publication

UNIVERSITY OF NEW SOUTH WALES

 

IMAGE: 

LENACAPAVIR CAUSES THE HIV CAPSID TO RUPTURE BEFORE IT CAN TRANSPORT ITS GENETIC MATERIAL TO THE HOST CELL NUCLEUS

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CREDIT: PUBLIC HEALTH IMAGE LIBRARY, CDC

Just over a year ago, the European Union and the US Food and Drug Administration approved a new anti-retroviral drug to treat human immunodeficiency virus (HIV) infections. Lenacapavir is the first drug available to patients that is designed to home in on the HIV’s protective armour – the HIV capsid.

An international team of researchers led by UNSW Sydney medical researchers now have the details on how this novel drug pushes the HIV capsid to breaking point, stopping the virus in its tracks. The molecular mechanisms that they uncovered are published in the journal eLife, and could help to refine and design more effective anti-viral therapies.

HIV encases its genetic material in a protein coat to safeguard the virus as it converts its genomic RNA into DNA enroute to the nucleus after entering the target cell. Developed by biopharmaceutical company Giliad Sciences, lenacapavir was designed to thwart this very protection afforded by the capsid. And this potent and long-acting drug is the first, and so far the only, approved anti-HIV therapy to do so.

“The fact that the capsid plays a central role in multiple stages of the viral life cycle, and therefore represents a really good drug target, is a concept that's only emerged in recent years,” said Professor Till Böcking, who led the team together with Dr David Jacques.

Building them tough to break them down

By combining cell infection studies with single-molecule imaging, the researchers showed how lenacapavir disrupted the HIV life cycle. Some theorised that the drug hardens the capsid to lock the virus in, thereby preventing it from establishing infection. Instead, the team saw that the capsid, fortified by the drug, actually became very brittle.

“What we found was that this hyper-stabilization actually led to a premature breakage of the capsid, before the virus can finish converting its RNA into DNA,” Professor Böcking said.

In the target cell, the capsid would rupture before the virus reaches the nucleus, leaving its genetic material exposed to the hostile environment in the host cell cytoplasm. To study the effect of lenacapavir on individual capsids over time, the team worked with non-infectious HIV-like particles produced by cells.

“With our microscope setup, we can look at the integrity of the capsids. By monitoring the release of fluorescent tags loaded into the capsid, we can work out exactly when it cracks,” said Dr Walsh, one of the study’s lead authors.

With Dr Leo James and other colleagues in the Laboratory of Molecular Biology in the UK, the team also examined the building of new capsids, recreating a process that would take place after newly made copies of the viral genome are bundled up for release from infected cells. They found that lenacapavir sabotaged capsid integrity at this phase of the HIV life cycle as well by accelerating the capsid construction to force construction errors. The deformed capsids that were produced were unable to close properly and would fail to shield the viral genome from attack.

This study not only settles the debate over whether capsid-targeting drugs strengthen or weaken the capsid, the uncovered mechanism could also be exploited for targeting other viruses that build capsids to shelter from host defences.

“Lenacapavir is orders of magnitude better than any other compound that targets the capsid. Our results give a really good blueprint for how this drug is able to be so incredibly effective,” said Dr Walsh.

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JOURNAL

eLife

DOI

10.7554/eLife.83605 

METHOD OF RESEARCH

Experimental study

ARTICLE TITLE

Pharmacologic hyperstabilisation of the HIV-1 capsid lattice induces capsid failure

ARTICLE PUBLICATION DATE

13-Feb-2024

ARACHNOPHOBIA TRIGGER; TOO LATE

Joro spiders well poised to populate cities

Study suggests invasive spider tolerates urban landscape better than most native spiders

Peer-Reviewed Publication

UNIVERSITY OF GEORGIA

 

IMAGE: 

A NEW UGA STUDY FOUND THE INVASIVE JORO SPIDER ISN'T PARTICULARLY PHASED BY THE VIBRATIONS AND NOISE OF CITY LIVING.

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CREDIT: (PHOTO BY UGA/DOROTHY KOZLOWSKI)

The Jorō (Joro) spider was first spotted stateside around 2013 and has since been spotted across Georgia and the Southeast. New research from the University of Georgia has found more clues as to why the spider has been so successful in its spread.

The study found the invasive orb-weaving spider is surprisingly tolerant of the vibrations and noise common in urban landscapes.

In this new study, researchers examined how Joro spiders can live next to busy roads, which are notably stressful environments for many animals.

The researchers found that while Joro spiders near busier roads are somewhat less likely to attack simulated prey, the spiders don’t seem to be hurting for it and clock in at about the same weight as their counterparts in less busy locations. That suggests the species can successfully compensate for its human-dominated landscape.

“If you’re a spider, you rely on vibrations to do your job and catch bugs,” said Andy Davis, corresponding author of the study and a research scientist in UGA’s Odum School of Ecology. “But these Joro webs are everywhere in the fall, including right next to busy roads, and the spiders seem to be able to make a living there. For some reason, these spiders seem urban tolerant.”

Busy roads don’t affect Joro spider health, weight

Joro spiders are regularly spotted in areas that native Georgia spiders don’t inhabit.

They build their golden webs between powerlines, on top of stoplights and even above the pumps at local gas stations—none of which are particularly peaceful spots.

This is what drew Davis and his team to study their behavior near roadsides.

Davis and a team of undergraduates from the Odum School used a tuning fork to simulate the vibrations caused by prey when caught in a spider’s web and then watched if the spiders attacked. Of the more than 350 trials, Joro spiders attacked the simulated prey 59% of the time.

The spiders in webs near busy roads attacked about half the time while those near lower traffic areas pounced 65% of the time.

Despite that slight difference, it doesn’t look like it’s affecting the spiders’ body mass or health.

“It looks like Joro spiders are not going to shy away from building a web under a stoplight or an area where you wouldn’t imagine a spider to be,” said Alexa Schultz, co-author of the study and a third-year ecology student at UGA. “I don’t know how happy people are going to be about it, but I think the spiders are here to stay.” Her undergraduate co-authors, Kade Stewart and Caitlin Phelan, agreed.

Joro spiders likely to spread beyond Southeast

In their native Japan, the East Asian Joro spider colonizes most of the country. Japan also has a very similar climate to the U.S. and is approximately the same latitude.

The present study builds on previous work from Davis’ lab that showed Joro spiders are well equipped to spread through most of the Eastern Seaboard due to their high metabolism and heart rate. The spiders are also cold tolerant, surviving brief freezes that kill off many of their orb-weaving cousins.

Their hardiness is one trait that’s enabled the spiders to explode in population stateside, with numbers easily in the millions now. The new research suggests that the Joros’ tolerance of urban vibrations and sounds is likely another factor in the species’ exponential growth.

But their spread shouldn’t be too alarming, the researchers said. The spiders are rather timid.

Published by Arthropoda, the study is available here.

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JOURNAL

Arthropoda

DOI

10.3390/arthropoda2010004 

ARTICLE TITLE

How Urban-Tolerant Are They? Testing Prey–Capture Behavior of Introduced Jorō Spiders (Trichonephila clavata) Next to Busy Roads

ARTICLE PUBLICATION DATE

13-Feb-2024

SPAGYRIC HERBALISM

Sandalwood oil by-product prevents prostate cancer development in mice

Natural compound decreases incidence of prostate tumors without weight loss or noticeable side effects

Peer-Reviewed Publication

FLORIDA ATLANTIC UNIVERSITY

 

IMAGE: 

Ajay Bommareddy, PH.D., SENIOR AUTHOR AND AN ASSOCIATE PROFESSOR OF PHARMACOLOGY, FAU SCHMIDT COLLEGE OF MEDICINE.

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CREDIT: FLORIDA ATLANTIC UNIVERSITY

Extracted from the core of sandalwood trees (santalum album tree), sandalwood oil has been used for many centuries by several cultures throughout the world for perfume, soaps, incense and candles. With its earthy sweet scent, this essential oil also is used in the food industry and topically in various cosmetic preparations.

Importantly, this natural oil is known for its health benefits and medicinal applications from antibacterial to anticancer because of its phytochemical constituents. In addition to containing esters, free acids, aldehydes, ketones and santenone, sandalwood oil primarily (90 percent or more) constitutes santalol – equal amounts of two compounds, alpha and beta-santalol.

Now, researchers from Florida Atlantic University’s Schmidt College of Medicine and collaborators are the first to demonstrate in vivo the chemo-preventive properties of alpha-santalol against prostate cancer development using a transgenic mouse model.

Results of the study, published in the journal Phytomedicine Plus, showed that administration of alpha-santalol decreased the incidence of prostate tumors by decreasing cell proliferation and inducing apoptosis, without causing weight loss or any noticeable side effects. Apoptosis, or programmed cell death, is a method the body uses to get rid of unneeded or abnormal cells such as cancer cells.

Findings revealed that the area occupied by normal tissue in alpha-santalol-treated mice was 53 percent compared to 12 percent in control mice. This suggests that administering alpha-santalol protected the normal tissue and delayed progression from prostatic intraepithelial neoplasia, a precancerous condition, to poorly differentiated carcinoma, a high-grade form of cancer where cancer cells and tissue look very abnormal. These results are significant because mortality in prostate cancer patients is mainly attributable to advanced stages of the disease.

In prior studies, the researchers demonstrated the efficacy of alpha-santalol in suppressing growth and inducing apoptotic cell death in cultured human prostate cancer cells. Based on these observations, they selected a genetically engineered mouse model that resembles many features similar to human prostate cancer, eliciting different lesion grades and cancer progression.

“Although our cellular studies provided important mechanistic insights, relevant in vivo models are vital for developing novel chemo-preventive agents for clinical use and to determine if alpha-santalol offers protection against prostate cancer development,” said Ajay Bommareddy, Ph.D., senior author and an associate professor of pharmacology in the Department of Biomedical Science, FAU Schmidt College of Medicine. “Prior to this new study, alpha-santalol’s in vivo efficacy against prostate cancer development had not yet been established.”

Additional findings of the current study showed alpha-santalol reduced the incidence of visible prostate tumors compared to control-treated mice. Only 11 percent in the treated group developed prostate tumors whereas more than half in the control group developed the tumors. The differences in urogenital and prostate weights were statistically significantly different in alpha-santalol-treated mice compared with controls. The average wet weight of urogenital tract in alpha-santalol treated mice was about 74.28 percent lower compared with control mice. Similarly, the average wet weight of the prostate gland was lower by 52.9 percent compared with control mice.

Prostate cancer is the second leading cause of cancer death in men in the United States. An estimated 288,300 new cases were diagnosed in American men last year with about 34,700 estimated deaths. 

Current treatment methods for prostate cancer include androgen ablation, chemotherapy, radiotherapy and radical prostatectomy, but are ineffective against advanced prostate cancers. Early detection and local therapy have resulted in improved outcomes but has been challenging with the management of advanced stages.

“Identifying agents that have the ability to selectively target cancerous cells and delay onset and progression of prostate cancer is greatly needed,” said Bommareddy. “Additional studies are essential to systemically explore the feasibility of alpha-santalol as a promising chemo-preventive and anti-tumor agent against human prostate cancer development and to elucidate the mechanisms surrounding the role of pro-apoptotic and antiapoptotic proteins.”

Study co-authors are John Oberlin Jr., PharmD; Kaitlyn Blankenhorn, PharmD; Sarah Hughes, PharmD; Erica Mabry, PharmD; Aaron Knopp, PharmD; Adam L. VanWert, PharmD, Ph.D., all with the Wilkes University Nesbitt School of Pharmacy; Chandradhar Dwivedi, Ph.D., South Dakota State University; Isaiah Pinkerton, a graduate of Wilkes University; and Linda Gutierrez, M.D., Wilkes University.   

- FAU -

About the Charles E. Schmidt College of Medicine:

FAU’s Charles E. Schmidt College of Medicine is one of approximately 156 accredited medical schools in the U.S. The college was launched in 2010, when the Florida Board of Governors made a landmark decision authorizing FAU to award the M.D. degree. After receiving approval from the Florida legislature and the governor, it became the 134th allopathic medical school in North America. With more than 70 full and part-time faculty and more than 1,300 affiliate faculty, the college matriculates 64 medical students each year and has been nationally recognized for its innovative curriculum. To further FAU’s commitment to increase much needed medical residency positions in Palm Beach County and to ensure that the region will continue to have an adequate and well-trained physician workforce, the FAU Charles E. Schmidt College of Medicine Consortium for Graduate Medical Education (GME) was formed in fall 2011 with five leading hospitals in Palm Beach County. The Consortium currently has five Accreditation Council for Graduate Medical Education (ACGME) accredited residencies including internal medicine, surgery, emergency medicine, psychiatry, and neurology.

 

About Florida Atlantic University:
Florida Atlantic University, established in 1961, officially opened its doors in 1964 as the fifth public university in Florida. Today, the University serves more than 30,000 undergraduate and graduate students across six campuses located along the southeast Florida coast. In recent years, the University has doubled its research expenditures and outpaced its peers in student achievement rates. Through the coexistence of access and excellence, FAU embodies an innovative model where traditional achievement gaps vanish. FAU is designated a Hispanic-serving institution, ranked as a top public university by U.S. News & World Report and a High Research Activity institution by the Carnegie Foundation for the Advancement of Teaching. For more information, visit www.fau.edu.

 

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JOURNAL

Phytomedicine Plus

DOI

10.1016/j.phyplu.2024.100523 

METHOD OF RESEARCH

Experimental study

SUBJECT OF RESEARCH

Animals

ARTICLE TITLE

Alpha-santalol, a derivative of sandalwood oil prevents development of prostate cancer in TRAMP mice

 

Irrigation strengthens climate resilience in Mali

Peer-Reviewed Publication

PNAS NEXUS

 

IMAGE: 

INTERVENTION SITES IN NORTHERN MALI.

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CREDIT: BENYISHAY ET AL

The installation of small-scale irrigation systems in communities in Mali led to lasting increases in agricultural productivity, decreases in local child malnutrition, and decreases in local conflict, providing resilience to climate change. Between 1999 and 2020, German development agencies installed hundreds of small-scale irrigation systems to pump water from the Niger River onto crops. Development agencies also made improvements to seasonally flooded depressions near rivers known as mares. Ariel BenYishay and colleagues gathered data using remote sensing, household surveys, and data from the Armed Conflict Location & Event Data Project. Using data from all three sources, the authors compared 1,000 locations before and after irrigation improvements. Irrigation increased the greenness of local areas by an average of 32% even 15 years later, mostly during the rainy season. Using standard models, the authors estimate that this enhanced greenness represents an increase in rice yield of approximately half a ton per hectare—an estimate that matches farmer reports. Most of the improvements were found around pump irrigation projects; improvements of the mares were less successful. Children living near pump irrigation projects were less likely to be stunted or wasted than children at pre-irrigation sites. Children who live 4–6km away, however, were found to be more nutritionally compromised than average. Finally, there was less conflict close to irrigated areas than in non-irrigated areas, perhaps because rebels spare project sites. According to the authors, pump irrigation will help buffer the effects of climate change, which is predicted to raise the average temperature in Mali by 2.0 to 4.6°C by 2080.

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JOURNAL

PNAS Nexus

ARTICLE TITLE

Irrigation strengthens climate resilience: Long-term evidence from Mali using satellites and surveys

ARTICLE PUBLICATION DATE

13-Feb-2024

Imagined Archive: Anthropological poetry at SAPIENS Magazine

UNIVERSITY OF CHICAGO PRESS JOURNALS

PRESS RELEASE
Contact: Chip Colwell
editor@sapiens.org

New York, NY – SAPIENS magazine is excited to share news of its 2024 poet-in-residence: Alma Simba. Through this position, Alma will use poetry to experiment with the idea of an imagined archive to explore the ways in which histories of Black African women are often rendered invisible.

“I am looking forward to the SAPIENS residency to explore this idea of a constructed archive,” Alma says. “SAPIENS’ anthropological focus and its unique approach to problematizing scholarly assumptions of the filed will allow me to engage with this notion of official narratives and the complexity of heritage and identity that is often ignored.”

Alma is a poet, historian, and writer based in Dar es Salaam, Tanzania. She is interested in the power of words in capturing the complexity of the human experience. At the same time, her work is also interested in moments where words are insufficient, particularly in instances of trauma, grief, and systemic erasure. Alma has an M.A. in history from the University of Dar es Salaam. Her areas of interest include histories of marginalized identities, heritage, memory, and Oral Traditions. Alma was a 2022 Sensitive Provenances Research Fellow at the University of Göttingen, where she engaged with ancestral human remains from Tanzania. The collection lacks sufficient biographic evidence—a source of ongoing trauma and difficulty for Tanzanians.

“I am moved by this idea of using poetry as an imaginative tool to fill the gaps where African women are overlooked completely. Poetry allows us to creatively visualize the past in a way that goes beyond statistics and dates,” Alma says. “Through this language, history can take a more human dimension—where the archive is not just dead ends and shadows but a chance to dream and creatively re-construct.”

She believes that through poetry and invention, people can go beyond the trauma of state-sanctioned colonial violence and envisage the possibility of healing and, perhaps, justice.

Alma is honored to be the next digital resident at SAPIENS. “Without this residency, I would not be able to explore in such a structured and supported way this idea of an imagined archive that I have been meditating on for years,” Alma relates. “I am excited about the poetic development I will receive during the residency and the practical insights from the SAPIENS team. The magazine is a one-of-a-kind platform that aligns with my approach of engaging with academic issues in nonacademic language. With this, I hope to engage a more global dimension to the SAPIENS audience and bring unseen histories to the forefront.”

This will be the fourth year of the program. SAPIENS’ outgoing poet-in-residence, Toiba Naseema, contributed an in-depth introduction about Indian-occupied Kashmir and three original poems with accompanying audio recordings and photos. Toiba also was a co-editor for a curated collection titled Poems of Witness and Possibility: Inside Zones of Conflict that began rolling out on January 29 of this year.

At the end of her residency, Toiba expressed that “SAPIENS is a great platform for exploring the lives of humans. I had a great time during the residency and learned a lot from the SAPIENS team. I really appreciate their inclusivity.” She added, “I believe during such hard times, SAPIENS sees the world through humanitarian eyes. Through the residency platform, I was able to represent my place, Kashmir, to the rest of the world via anthropological poetry. I believe occupation will come to an end when people connect and show solidarity via platforms like SAPIENS. I thank the team for bestowing on me this position, and I hope the magazine will sustain its motive of awakening the world toward justice.”

In 2022, Jason Vasser-Elong served as the poet-in-resident, contributing six original poems with accompanying audio recordings. Jason also served as a co-editor for the Indigenizing What It Means to Be Human project, a collection of 19 poems and stories. A Q&A with him can be found on SAPIENS’ website: “Rhyme & Reason: Poetry as a Cultural and Communal Bridge.”

SAPIENS’ inaugural poet-in-residence in 2020–2021 was Justin D. Wright (as of 2023, Día Joy Wright) a doctoral student in sociocultural anthropology at American University. During their tenure, Justin contributed original autoethnographic poems. They also served as a co-editor of the Lead Me to Life: Voices of the African Diaspora collection and a co-author of the article “What Is Anthropological Poetry?”

Anthropological poems bring readers insights, emotions, aspirations, and interventions from skilled observers of the human and nonhuman worlds to reflect on “what it means to be vitally human and to make sense of the human experience.”

CONTACT:
Christine Weeber, Poetry Editor

SAPIENS Magazine
editor@sapiens.org