Hematology and Clinical Chemistry Reference Ranges for Laboratory-Bred Natal Multimammate Mice (Mastomys natalensis)

Laboratory-controlled physiological data for the multimammate rat (Mastomys natalensis) are scarce, despite this species being a known reservoir and vector for zoonotic viruses, including the highly pathogenic Lassa virus, as well as other arenaviruses and many species of bacteria. For this reason, M. natalensis is an important rodent for the study of host-virus interactions within laboratory settings. Herein, we provide basic blood parameters for age- and sex-distributed animals in regards to blood counts, cell phenotypes and serum chemistry of a specific-pathogen-monitored M.natalensis breeding colony, to facilitate scientific insight into this important and widespread rodent species.

Download Full-text

Association between faecal shedding of feline coronavirus and serum α1-acid glycoprotein sialylation

Journal of Feline Medicine and Surgery ◽

10.1016/j.jfms.2008.04.004 ◽

2008 ◽

Vol 10 (5) ◽

pp. 514-518 ◽

Cited By ~ 15

Author(s):

Saverio Paltrinieri ◽

Maria E. Gelain ◽

Fabrizio Ceciliani ◽

Alba M. Ribera ◽

Mara Battilani

Keyword(s):

Sialic Acid ◽

Quantitative Polymerase Chain Reaction ◽

Acid Glycoprotein ◽

Viral Shedding ◽

Lectin Staining ◽

Specific Pathogen ◽

Group B ◽

Host Virus Interactions ◽

Virus Interactions ◽

Feline Coronavirus

The sialylation pattern of serum α1-acid glycoprotein (AGP) in non-symptomatic cats infected by feline coronavirus (FCoV) and its possible relationship with the amount of FCoVs shed in faeces were investigated. Blood from three specific pathogen-free cats (group A) and from 10 non-symptomatic FCoV-positive cats from catteries with low (group B, three cats) or high (group C, seven cats) levels of faecal shedding were collected monthly. AGP was purified from serum and Western blotting followed by lectin-staining of α(2,3)-linked and α(2,6)-linked sialic acid. Faecal shedding was quantified in group C by quantitative polymerase chain reaction. Variations of AGP sialylation were recorded only in cats from group C, on which viral shedding peaked before the occurrence of feline infectious peritonitis (FIP) in the cattery, and decreased 1 month later, when serum AGP had an increase of α(2,3)-linked sialic acid. These results suggest that hypersialylation of AGP may be involved in host–virus interactions.

Download Full-text

Host-virus interactions: Lessons from the model organismDrosophila melanogaster

10.1603/ice.2016.92693 ◽

2016 ◽

Author(s):

Jean-Luc Imler

Keyword(s):

Host Virus Interactions ◽

Virus Interactions

Download Full-text

The molecular footprints of COVID-19

Turkish Journal of Biochemistry ◽

10.1515/tjb-2020-0255 ◽

2020 ◽

Vol 45 (3) ◽

pp. 241-248

Author(s):

Engin Yilmaz ◽

Yakut Akyön ◽

Muhittin Serdar

Keyword(s):

Reaction Time ◽

Changing Environment ◽

The Third ◽

The Past ◽

The People ◽

The World ◽

The Future ◽

Host Virus Interactions ◽

Virus Interactions

AbstractCOVID-19 is the third spread of animal coronavirus over the past two decades, resulting in a major epidemic in humans after SARS and MERS. COVID-19 is responsible of the biggest biological earthquake in the world. In the global fight against COVID-19 some serious mistakes have been done like, the countries’ misguided attempts to protect their economies, lack of international co-operation. These mistakes that the people had done in previous deadly outbreaks. The result has been a greater economic devastation and the collapse of national and international trust for all. In this constantly changing environment, if we have a better understanding of the host-virus interactions than we can be more prepared to the future deadly outbreaks. When encountered with a disease which the causative is unknown, the reaction time and the precautions that should be taken matters a great deal. In this review we aimed to reveal the molecular footprints of COVID-19 scientifically and to get an understanding of the pandemia. This review might be a highlight to the possible outbreaks.

Download Full-text

Experimental Morogoro Virus Infection in Its Natural Host, Mastomys natalensis

Viruses ◽

10.3390/v13050851 ◽

2021 ◽

Vol 13 (5) ◽

pp. 851

Author(s):

Chris Hoffmann ◽

Stephanie Wurr ◽

Elisa Pallasch ◽

Sabrina Bockholt ◽

Toni Rieger ◽

...

Keyword(s):

Persistent Infection ◽

Virus Transmission ◽

Host Population ◽

Natural Host ◽

Lassa Virus ◽

Mastomys Natalensis ◽

Natural Hosts ◽

History Of ◽

Morogoro Virus ◽

The Impact

Natural hosts of most arenaviruses are rodents. The human-pathogenic Lassa virus and several non-pathogenic arenaviruses such as Morogoro virus (MORV) share the same host species, namely Mastomys natalensis (M. natalensis). In this study, we investigated the history of infection and virus transmission within the natural host population. To this end, we infected M. natalensis at different ages with MORV and measured the health status of the animals, virus load in blood and organs, the development of virus-specific antibodies, and the ability of the infected individuals to transmit the virus. To explore the impact of the lack of evolutionary virus–host adaptation, experiments were also conducted with Mobala virus (MOBV), which does not share M. natalensis as a natural host. Animals infected with MORV up to two weeks after birth developed persistent infection, seroconverted and were able to transmit the virus horizontally. Animals older than two weeks at the time of infection rapidly cleared the virus. In contrast, MOBV-infected neonates neither developed persistent infection nor were able to transmit the virus. In conclusion, we demonstrate that MORV is able to develop persistent infection in its natural host, but only after inoculation shortly after birth. A related arenavirus that is not evolutionarily adapted to M. natalensis is not able to establish persistent infection. Persistently infected animals appear to be important to maintain virus transmission within the host population.

Download Full-text

Human stem cell models to study host–virus interactions in the central nervous system

Nature Reviews Immunology ◽

10.1038/s41577-020-00474-y ◽

2021 ◽

Author(s):

Oliver Harschnitz ◽

Lorenz Studer

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Stem Cell ◽

Human Stem Cell ◽

Cell Models ◽

The Central Nervous System ◽

Host Virus Interactions ◽

Virus Interactions ◽

Stem Cell Models

Download Full-text

Poxviral Strategies to Overcome Host Cell Apoptosis

Pathogens ◽

10.3390/pathogens10010006 ◽

2020 ◽

Vol 10 (1) ◽

pp. 6

Author(s):

Chathura D. Suraweera ◽

Mark G. Hinds ◽

Marc Kvansakul

Keyword(s):

Viral Infections ◽

B Cell Lymphoma ◽

Intrinsic Apoptosis ◽

Host Cell Apoptosis ◽

Successful Infection ◽

Infected Cells ◽

Host Virus Interactions ◽

Almost All ◽

Virus Interactions ◽

Multicellular Organisms

Apoptosis is a form of cellular suicide initiated either via extracellular (extrinsic apoptosis) or intracellular (intrinsic apoptosis) cues. This form of programmed cell death plays a crucial role in development and tissue homeostasis in multicellular organisms and its dysregulation is an underlying cause for many diseases. Intrinsic apoptosis is regulated by members of the evolutionarily conserved B-cell lymphoma-2 (Bcl-2) family, a family that consists of pro- and anti-apoptotic members. Bcl-2 genes have also been assimilated by numerous viruses including pox viruses, in particular the sub-family of chordopoxviridae, a group of viruses known to infect almost all vertebrates. The viral Bcl-2 proteins are virulence factors and aid the evasion of host immune defenses by mimicking the activity of their cellular counterparts. Viral Bcl-2 genes have proved essential for the survival of virus infected cells and structural studies have shown that though they often share very little sequence identity with their cellular counterparts, they have near-identical 3D structures. However, their mechanisms of action are varied. In this review, we examine the structural biology, molecular interactions, and detailed mechanism of action of poxvirus encoded apoptosis inhibitors and how they impact on host–virus interactions to ultimately enable successful infection and propagation of viral infections.

Download Full-text

Role of Mitochondria in Viral Infections

Life ◽

10.3390/life11030232 ◽

2021 ◽

Vol 11 (3) ◽

pp. 232

Author(s):

Srikanth Elesela ◽

Nicholas W. Lukacs

Keyword(s):

Viral Infections ◽

Mitochondrial Dynamics ◽

The Body ◽

Viral Diseases ◽

Multiple Organs ◽

Innate Immune Signaling ◽

Mitochondrial Functions ◽

Host Virus Interactions ◽

Virus Interactions

Viral diseases account for an increasing proportion of deaths worldwide. Viruses maneuver host cell machinery in an attempt to subvert the intracellular environment favorable for their replication. The mitochondrial network is highly susceptible to physiological and environmental insults, including viral infections. Viruses affect mitochondrial functions and impact mitochondrial metabolism, and innate immune signaling. Resurgence of host-virus interactions in recent literature emphasizes the key role of mitochondria and host metabolism on viral life processes. Mitochondrial dysfunction leads to damage of mitochondria that generate toxic compounds, importantly mitochondrial DNA, inducing systemic toxicity, leading to damage of multiple organs in the body. Mitochondrial dynamics and mitophagy are essential for the maintenance of mitochondrial quality control and homeostasis. Therefore, metabolic antagonists may be essential to gain a better understanding of viral diseases and develop effective antiviral therapeutics. This review briefly discusses how viruses exploit mitochondrial dynamics for virus proliferation and induce associated diseases.

Download Full-text