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How do the outcomes of viral coinfections vary across host species? – News-Medical.Net

In a recent study published in the journal PLOS Pathogens, researchers investigated the outcomes of coinfections of two viruses — Drosophila C Virus (DCV) and Cricket Paralysis Virus (CrPV) in 25 inbred lines of Drosophila melanogaster and 47 other host species belonging to the Drosophilidae family.

Study: Investigating the outcomes of virus coinfection within and across host species. Image Credit: kajornyot wildlife photography / ShutterstockStudy: Investigating the outcomes of virus coinfection within and across host species. Image Credit: kajornyot wildlife photography / Shutterstock


The infection of a host with multiple pathogenic species or lineages is common in the real world, and factors such as virulence, clinical outcomes, viral loads, and transmission rates of the pathogens can change based on the interactions between infecting pathogens. Furthermore, the interactions between the pathogens can also change the dynamics of the disease at a population level, such as the prevalence of one virus influencing the spread of the other or established pathogens preventing the establishment of a novel virus in the population.

These interactions between coinfecting pathogens result in changing selection pressures on the pathogens and the host, which drives the genetic diversity within the pathogen population. Coinfecting pathogens can interact directly with each other by inhibiting or modulating the other pathogen’s gene expression or producing toxins or hybrid virions, or indirectly through interactions with the host immune system or competing for the resources within the host. Research indicates that host genotypes and the dietary choices of the host influence the outcomes of the coinfection. However, the outcomes of coinfections across host species remain largely understudied.

About the study

In the present study, the researchers used two Cripaviruses, DCV, and CrPV, to coinfect different lines of Drosophila melanogaster and 47 species from the family Drosophilidae. The viral loads for single infections and coinfections were compared across the Drosophila lines and Drosophilidae hosts. Analyzing the viral loads and the difference in viral loads between single infections and coinfections helped quantify the host susceptibility to DCV and CrPV across phylogenetic and genetic components. It also helped understand the direction and strength of the interactions between the two viruses during the coinfection.

CrPV and DCP are similar in their interactions with the host Drosophila melanogaster in that they both activate the immune deficiency (IMD) pathway and are targeted by the antiviral ribonucleic acid (RNA) interference (RNAi) pathway. Both viruses encode antiviral RNAi inhibitors to prevent antiviral RNAi action, but these inhibitors bind to different targets. Furthermore, differences also exist in phenotypic changes induced by the viruses. DCV infections cause food to accumulate in the Drosophila fly crop, resulting in intestinal obstruction and subsequent nutritional stress, which is not observed in CrPV infections.

Based on the differences in RNAi inhibitor targets and the phenotypic changes induced by the virus in the host, the interactions between DCVp and CrPV could be indirect via the transactivation of the antiviral gene expression in the host, suppression of antiviral RNAi, or resource competition. It could directly suppress the host immune system and enhance the replication and growth of both viruses or result in lower viral loads of one of the viruses.

Publicly available sequences for specific genes for the hosts were used to reconstruct the host phylogeny, while RNA extracted from infected Drosophila was used to carry out quantitative reverse transcription polymerase chain reaction (qRT-PCR) for viral markers to determine the viral load.


The results reported that across the 25 inbred lines of Drosophila melanogaster, interactions between the two viruses resulted in a 2.5-fold decrease in the viral loads of CrPV along with a three-fold increase in DCV accumulation during coinfections as compared to a single infection. The genetic basis of the host did not seem to influence interactions between the two viruses during coinfections.

Furthermore, the susceptibility to the viruses during the coinfection did not seem to be influenced by variations in host genetics, and in a large number of the Drosophilidae species, no interactions were noticed between CrPV and DCV during coinfections. While during single infections, the genetic variation across the host species was associated with varying susceptibility, similar associations between the genetic component of the host and either the changing susceptibility to a coinfecting virus or the strength of the viral interactions during coinfections were not observed.


Overall, the findings indicated that while interactions between CrPV and DCV during coinfections in Drosophila melanogaster result in an increase in the viral loads of DCV and a decrease in the CrPV viral loads, the host genetics do not seem to influence these interactions. Furthermore, the evolutionary relationships or the genetic variation between the host species did not influence the changes in interactions between the viruses during single infections and coinfections.

Journal reference:

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Phenomenal phytoplankton: Scientists uncover cellular process behind oxygen production – EurekAlert


image: A composition image of diatoms, single-celled algae famous for their ornamental cell walls made of silica.
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Credit: Daniel Yee

Take a deep breath. Now take nine more. According to new research, the amount of oxygen in one of those 10 breaths was made possible thanks to a newly identified cellular mechanism that promotes photosynthesis in marine phytoplankton.

Described as “groundbreaking” by a team of researchers at UC San Diego’s Scripps Institution of Oceanography, this previously unknown process accounts for between 7% to 25% of all the oxygen produced and carbon fixed in the ocean. When also considering photosynthesis occuring on land, researchers estimated that this mechanism could be responsible for generating up to 12% of the oxygen on the entire planet.

Scientists have long recognized the significance of phytoplankton—microscopic organisms that drift in aquatic environments—due to their ability to photosynthesize. These tiny oceanic algae form the base of the aquatic food web and are estimated to produce around 50% of the oxygen on Earth.

The new study, published May 31 in the journal Current Biology, identifies how a proton pumping enzyme (known as VHA) aids in global oxygen production and carbon fixation from phytoplankton.

“This study represents a breakthrough in our understanding of marine phytoplankton,” said lead author Daniel Yee, who conducted the research while a PhD student at Scripps Oceanography and currently serves as a joint postdoctoral researcher at the European Molecular Biology Laboratory and University of Grenoble Alpes in France. “Over millions of years of evolution, these small cells in the ocean carry out minute chemical reactions, in particular to produce this mechanism that enhances photosynthesis, that shaped the trajectory of life on this planet.”

Working closely with Scripps physiologist Martín Tresguerres, one of his co-advisors, and other collaborators at Scripps and the Lawrence Livermore National Laboratory, Yee unraveled the complex inner workings of a specific group of phytoplankton known as diatoms, which are single-celled algae famous for their ornamental cell walls made of silica.

Understanding the “proton pump” enzyme

Previous research in the Tresguerres Lab has worked to identify how VHA is used by a variety of organisms in processes critical to life in the oceans. This enzyme is found in nearly all forms of life, from humans to single-celled algae, and its basic role is to modify the pH level of the surrounding environment.

“We imagine proteins as Lego blocks,” explained Tresguerres, a study co-author. “The proteins always do the same thing, but depending on what other proteins they are paired with, they can achieve a vastly different function.”

In humans, the enzyme aids kidneys in regulating blood and urine functions. Giant clams use the enzyme to dissolve coral reefs, where they secrete an acid that bores holes in the reef to take shelter. Corals use the enzyme to promote photosynthesis by their symbiotic algae, while deep-sea worms known as Osedax use it to dissolve the bones of marine mammals, such as whales, so they can consume them. The enzyme is also present in the gills of sharks and rays, where it is part of a mechanism that regulates blood chemistry. And in fish eyes, the proton pump helps deliver oxygen that enhances vision. 

Looking at this previous research, Yee wondered how the VHA enzyme was being used in phytoplankton. He set out to answer this question by combining high-tech microscopy techniques in the Tresguerres Lab and genetic tools developed in the lab of the late Scripps scientist Mark Hildebrand, who was a leading expert on diatoms and one of Yee’s co-advisors.

Using these tools, he was able to label the proton pump with a fluorescent green tag and precisely locate it around chloroplasts, which are known as “organelles” or specialized structures within diatom cells. The chloroplasts of diatoms are surrounded by an additional membrane compared to other algae, enveloping the space where carbon dioxide and light energy are converted into organic compounds and released as oxygen.

“We were able to generate these images that are showing the protein of interest and where it is inside of a cell with many membranes,” said Yee. “In combination with detailed experiments to quantify photosynthesis, we found that this protein is actually promoting photosynthesis by delivering more carbon dioxide, which is what the chloroplast uses to produce more complex carbon molecules, like sugars, while also producing more oxygen as a by-product.”

Connection to evolution

Once the underlying mechanism was established, the team was able to connect it to multiple aspects of evolution. Diatoms were derived from a symbiotic event between a protozoan and an algae around 250 million years ago that culminated into the fusing of the two organisms into one, known as symbiogenesis. The authors highlight that the process of one cell consuming another, known as phagocytosis, is widespread in nature. Phagocytosis relies on the proton pump to digest the cell that acts as the food source. However, in the case of diatoms, something special occurred in which the cell that was eaten didn’t get fully digested.

“Instead of one cell digesting the other, the acidification driven by the proton pump of the predator ended up promoting photosynthesis by the ingested prey,” said Tresguerres. “Over evolutionary time, these two separate organisms fused into one, for what we now call diatoms.”

Not all algae have this mechanism, so the authors think that this proton pump has given diatoms an advantage in photosynthesis. They also note that when diatoms originated 250 million years ago, there was a big increase in oxygen in the atmosphere, and the newly discovered mechanism in algae might have played a role in that.

The majority of fossil fuels extracted from the ground are believed to have originated from the transformation of biomass that sank to the ocean floor, including diatoms, over millions of years, resulting in the formation of oil reserves. The researchers are hopeful that their study can provide inspiration for biotechnological approaches to improve photosynthesis, carbon sequestration, and biodiesel production. Additionally, they think it will contribute to a better understanding of global biogeochemical cycles, ecological interactions, and the impacts of environmental fluctuations, such as climate change.

“This is one of the most exciting studies in the field of symbiosis in the past decades and it will have a large impact on future research worldwide,” said Tresguerres.

Additional co-authors include Raffaela Abbriano, Bethany Shimasaki, Maria Vernet, Greg Mitchell, and the late Mark Hildebrand of Scripps Oceanography; Ty Samo, Xavier Mayali, and Peter Weber of the Lawrence Livermore National Laboratory; and Johan Decelle of University of Grenoble Alpes.

The authors did not receive any funding for this study. Yee’s doctoral studies at Scripps Oceanography were supported by the Scripps Fellowship, the NIH training grant, and the Ralph Lewin Graduate Fellowship. Funds by UC San Diego’s Arthur M. and Kate E. Tode Research Endowment in Marine Biological Sciences supported the purchase of a microscope that was essential for the research.

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Further link identified between autoimmunity and schizophrenia – EurekAlert

Cell-based assay to detect the anti-NRXN1 autoantibody

image: NRXN1 is induced only in green cells (HeLa cells). Serum from patients with anti-NRXN1 autoantibody react only to green cells (framed in red).
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Credit: Department of Psychiatry and Behavioral Sciences, TMDU

Researchers from Tokyo Medical and Dental University (TMDU) identify a protein in some people with schizophrenia that causes schizophrenia-like features in mice

Tokyo, Japan – Links have been reported between schizophrenia and proteins produced by the immune system that can act against one’s own body, known as autoantibodies. In a study published last month in Brain Behavior and Immunity, Japanese researchers identified autoantibodies that target a ‘synaptic adhesion protein’, neurexin 1α, in a subset of patients with schizophrenia. When injected into mice, the autoantibodies caused many schizophrenia-related changes.

What is a synaptic protein, and why might it be linked to schizophrenia? Synaptic adhesion proteins are specialized proteins that bind to create physical connections between brain cells. These connections, called synapses, allow the cells to communicate by passing molecules back and forth. Both synapses and autoimmunity are known to be associated with schizophrenia, so the research team from Tokyo Medical and Dental University (TMDU) decided to investigate autoantibodies that target synaptic proteins in patients with schizophrenia.

“In around 2% of our patient population, we identified autoantibodies against the synaptic protein neurexin 1α, which is expressed by one cell in the synapse and binds to proteins known as neuroligins on the other cell in the synapse,” says lead author of the study Hiroki Shiwaku. “Once we had identified these autoantibodies, we wanted to see if they were able to cause schizophrenia-related changes.”

To do this, the researchers isolated autoantibodies from some of the patients with schizophrenia and injected them into the cerebrospinal fluid of mice, so that the autoantibodies would travel into the brain. In these mice, the autoantibodies blocked neurexin 1α and neuroligin binding and altered some related synaptic properties. The administration of these autoantibodies also resulted in fewer synapses in the brains of mice and schizophrenia-related behaviors, such as reduced social behavior toward unfamiliar mice and reduced cognitive function.

“Together, our results strongly suggest that autoantibodies against neurexin 1α can cause schizophrenia-related changes, at least in mice,” explains Hiroki Shiwaku. “These autoantibodies may therefore represent a therapeutic target for a subset of patients with schizophrenia.”

Schizophrenia has a wide variety of both symptoms and treatment responses, and many patients have symptoms that are resistant to currently available treatment options. Therefore, the identification of possible disease-causing autoantibodies is important for improving symptom control in patients with schizophrenia. It is hoped that the results of this investigation will allow patients with autoantibodies that target neurexin 1α—all of whom were resistant to antipsychotic treatment in the present study—to better control their symptoms in the future.


The article, “Analyzing schizophrenia-related phenotypes in mice caused by autoantibodies against NRXN1α in schizophrenia,” was published in Brain Behavior and Immunity at DOI: 10.1016/j.bbi.2023.03.028

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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New variants of human metapneumovirus surge in Spain post-COVID, highlighting evolution and impact – News-Medical.Net

An important aetiologic agent of upper respiratory tract infection (URTI) and lower respiratory tract infection (LRTI) in adults and children is the human metapneumovirus (HMPV). A recent Journal of Infection study explores the genetic diversity, prevalence, and evolutionary dynamics of HMPV.

Study: The emergence, impact, and evolution of human metapneumovirus variants from 2014 to 2021 in Spain. Image Credit: VO IMAGES / Study: The emergence, impact, and evolution of human metapneumovirus variants from 2014 to 2021 in Spain. Image Credit: VO IMAGES /


HMPV belongs to the Pneumoviridae family and causes similar symptomatology as the human respiratory syncytial virus (HRSV). HMPV is a negative-sensed, lineal, enveloped, and single-stranded ribonucleic acid (RNA) virus that can be classified into HMPV-A and HMPV-B genotypes, with its subgenotypes including A1, A2 (A2a, A2b, and A2c lineages), B1, and B2 (B2a and B2b lineages).

The genome of HMPV consists of eight genes encoding nine proteins. The scheme in which the proteins are encoded is 3’-N-P-M-F-M2(M2–1/M2–2)- SH-G-L-5’.

Recently, in the attachment glycoprotein’s (G) ectodomain,  180- and 111-nucleotide duplications have been associated with LRTI and immune evasion in adulthood. 

About the study

The current study aimed to characterize the evolutionary dynamics and genetic diversity of HMPV in adult and pediatric patients at a university hospital in Barcelona in the seasons between 2014-2015 and 2020-2021.

Laboratory-confirmed HMPV was characterized based on partial-coding G gene sequences. For the assembly of nucleotide sequences, the MEGA.v6.0 was used.

Phylogenetic trees were constructed based on the lowest Bayesian information criterion score. These trees were evaluated with 1,000 bootstrap resamplings. Whole genome sequencing (WGS) was performed with Illumina, and evolutionary analyses with Nextstrain and Datamonkey.

Key findings

Consistent with other studies, the prevalence of HMPV in pre-pandemic years was similar, with an annual seasonal pattern and clear peak. However, the start of the coronavirus disease 2019 (COVID-19) pandemic disrupted the circulation of HMPV. From the summer of 2020, enveloped viruses were circulating; however, HRSV or HMPV were not dominant.

In the summer of 2021, HMPV and HRSV were again in circulation and caused two epidemic peaks, the second of which started in the autumn. This could be due to a lack of viral interference at that time or the relaxation of preventive measures by Spanish people. During the second peak, the prevalence of HMPV was higher compared to previous seasons, likely because two generations had not yet experienced primary infection.

The most common co-detections were adenovirus, rhinovirus, bocavirus, and enterovirus. The co-detection rate increased after the COVID-19 pandemic, and a change was observed in most common co-detected viruses.

HMPV had shown a higher incidence among children under two years of age in pre-pandemic seasons; however, this changed during the pandemic. There was also a higher tendency of male infants to be affected. In contrast, in the adult population, females and individuals 50 years of age or older were more likely to be infected.

A pattern of cyclic shifts of predominance with respect to the circulation of HMPV-A was observed. In addition, an increasing prevalence of A2c viruses carrying duplications was observed, with A2c180dup first described, followed by A2c111dup. The dominance of A2c111dup indicates that the 180-nucleotide duplication covers much of the F protein, which could impact membrane fusion and prevent virus replication.

Consistent with the rise in prevalence of A2c variants and their dominance during the COVID-19 pandemic, an increase in the morbidity of HMPV infections had also been described at the end of the 2009 influenza A(H1N1)pdm09 pandemic. At this time, A2c exhibited a higher mean genetic distance and immune evasive characteristics that contributed to its aggressive predominance.


HMPV affected both pediatric and adult populations and showed significant morbidity throughout the study period. The HMPV epidemic was disrupted by the COVID-19 pandemic in 2020, which led to two unexpected peaks later in the summer and autumn of 2021.

WGS showed the high conservation of the F protein and rich diversity in G protein, thus indicating the necessity for steric shielding of G over F. The current study is an effective example of virological surveillance of a non-HRSV or influenza respiratory virus. It provides crucial information on the real-time evolution of HMPV and its impact on public health.

Journal reference:
  • Pinana, M., Gonzalez-Sanchez, A., Andres, C., et al. (2023) The emergence, impact, and evolution of human metapneumovirus variants from 2014 to 2021 in Spain. Journal of Infection. doi:10.1016/j.jinf.2023.05.004

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