Scientists discover new method Ebola virus uses to infect cells - Texas Biomed
Ebola virus.
For example, as researchers from the Texas Biomedical Research Institute (Texas Biomed) have discovered, the nasty little ebola virus uses a sneaky back-door approach to pass from cell to cell in a way which keeps it hidden from our immune system. Instead, it usurps the system our cells use to pass substances like proteins, nutrients and RNA from one cell to another via a network of nanotubes.
What is the Ebola Virus and what does it do to its victims? Ebola virus disease (EVD) is a severe and often fatal illness caused by the Ebola virus, a member of the Filoviridae family. The virus was first identified in 1976 when outbreaks occurred in Sudan and the Democratic Republic of Congo. Since then, sporadic outbreaks have occurred in Central and West African countries.Other viruses infect a cell, usurp the cell's replication processes to make more copies of themselves, then kill the cell to liberate virus particles into the tissues where they can invade and destroy other cells, so exposing themselves to attack by antibodies and T-cells from the immune system while training the immune system to recognise them.
Ebola virus primarily spreads through direct contact with the blood, secretions, organs, or other bodily fluids of infected animals (such as bats and primates) and with surfaces and materials contaminated with these fluids. Once the virus is introduced into the human population, it can spread from person to person through direct contact with the blood, secretions, organs, or other bodily fluids of infected people, as well as with surfaces and materials contaminated with these fluids.
Here are key features of Ebola virus and its effects on victims:It's important to note that while Ebola virus is a serious and potentially deadly disease, it is not as easily transmitted as some other infectious diseases, such as the flu or the common cold. Outbreaks are typically limited in scope and are contained through public health measures. Global efforts, including vaccination and improved healthcare infrastructure, aim to prevent and control the spread of the virus.
- Symptoms: The onset of symptoms is abrupt and includes fever, severe headache, muscle pain, fatigue, diarrhea, vomiting, abdominal pain, and unexplained bleeding or bruising.
- Severity: Ebola virus disease can be severe and has a high mortality rate, with death rates ranging from 25% to 90% in past outbreaks. The severity of the disease depends on various factors, including the strain of the virus and the patient's overall health.
- Incubation Period: The incubation period for Ebola virus disease is typically 2 to 21 days, and individuals are not contagious until they develop symptoms.
- Transmission: The virus is primarily transmitted through direct contact with the blood, secretions, organs, or other bodily fluids of infected individuals. Transmission can occur through broken skin or mucous membranes, such as the eyes, nose, or mouth.
- Treatment: There is no specific antiviral treatment for Ebola virus disease. Supportive care, including maintaining hydration and electrolyte balance, is crucial. Patients with severe cases may require intensive care.
- Prevention: Prevention measures include practicing good hygiene, avoiding contact with the blood or bodily fluids of infected individuals, using personal protective equipment (such as gloves and masks), and implementing safe burial practices.
Ebola, on the other hand, slips unnoticed along the communicating network of nanotubes where they are safe from our antibodies, so safely infecting neighbouring cells and eventually reaching cells and structures that are isolated from the immune system, like the fluid in our eyeballs, where it can lurk ready to launch another attack even if we recover from the first assault.
This recent discovery of the Texas Biomed team was published open access in the Journal of Infectious Diseases. As a Texas Biomed news article explains:
Understanding how viruses travel once inside the human body is critical to develop effective drugs and therapies that can stop viruses in their tracks. Scientists at Texas Biomedical Research Institute (Texas Biomed) recently published findings in the Journal of Infectious Diseases indicating that Ebola virus creates and uses intercellular tunnels to move from cell to cell and evade treatments.
Specifically, the virus is generating something called tunneling nanotubes – dynamic connections between cells that allow the cells to communicate by exchanging particles over relatively long distances, up to 200 microns. While these structures have been shown to play a prominent role in promoting neurodegenerative diseases, cancer, HIV-1 and influenza, Dr. Shtanko is the first to investigate their role in disseminating Ebola virus.Our findings suggest that the virus can create its hiding place, hide and then move to new cells and replicate. When we launched this project a couple of years ago, we thought the general model of spread of Ebola virus infection – where a viral particle infects a cell, replication begins, new virus particles are made and released into the body to infect neighboring cells – was a bit too simplistic.
Importantly, we observed that Ebola virus infection could spread in cultures treated with virus entry inhibitors or therapeutic treatments that stop viruses from entering a cell
Assistant Professor Dr Olena Shtanko, PhD, senior author.
Host-Pathogen Interactions
Texas Biomedical Research Institute, San Antonio, Texas, USA.
Using state-of-the-art technology with live scanning electron and high-resolution 3D-microscopy, Dr. Shtanko and her team showed that Ebola virus infection in cells enhanced the formation of tunneling nanotubes containing viral particles. The tunneling nanotubes then promoted the transfer of these particles to other cells. Notably, the full virus was not required to trigger nanotube formation, only small sections of the virus coding for individual proteins were needed.
This happened even in the presence of treatments meant to stop Ebola virus.
How exactly Ebola virus particles are transported through tunneling nanotubes is still an open question. Dr. Shtanko and her team plan to try to find answers using advanced technologies such laser microdissection, mass spectrometry and low-abundance RNA sequencing. They will also explore if related viruses, including deadly Sudan and Marburg viruses, exploit the same mechanism to spread infection. In collaboration with Texas Biomed Professor Ricardo Carrion, Jr., PhD, the team will analyze tissues from animal models for virus-containing nanotubes.
AbstractAltogether then, another example of how, if, as creationists insist, these organisms are too complex to have evolved and the only entity capable of designing them is their imaginary magic friend, then their imaginary magic friend is a pestilential sadist who enjoys making people sick and die.
Ebola virus (EBOV) disease is marked by rapid virus replication and spread. EBOV enters the cell by macropinocytosis and replicates in the cytoplasm, and nascent virions egress from the cell surface to infect neighboring cells. Here, we show that EBOV uses an alternate route to disseminate: tunneling nanotubes (TNTs). TNTs, an actin-based long-range intercellular communication system, allows for direct exchange of cytosolic constituents between cells. Using live, scanning electron, and high-resolution quantitative 3-dimensional microscopy, we show that EBOV infection of primary human cells results in the enhanced formation of TNTs containing viral nucleocapsids. TNTs promote the intercellular transfer of nucleocapsids in the absence of live virus, and virus could replicate in cells devoid of entry factors after initial stall. Our studies suggest an alternate model of EBOV dissemination within the host, laying the groundwork for further investigations into the pathogenesis of filoviruses and, importantly, stimulating new areas of antiviral design.
Ebola virus (EBOV) disease is characterized by an exceptionally efficient spread of uncontrolled viral replication in host tissues, evasion of host immune defenses, and persistence in immune-privileged sites. Macrophages are among the initial cells targeted by EBOV [1]. EBOV propagates infection through the cell-free form, where virus particles enter the cell by macropinocytosis, replicate in the cytoplasm, and then egress from the cell surface to infect new cells [2–4]. EBOV is an enveloped virus with a negative-strand RNA genome. The glycoprotein (GP) mediates the entry of cell-free virions. Nucleoprotein (NP) forms complexes with VP35, VP30, and the RNA-dependent RNA polymerase L to facilitate virus genome replication and transcription. NP, VP35, and VP24 proteins are required for proper nucleocapsid formation. The matrix protein (VP40) is the main driving force for EBOV budding at the cell surface from virus-induced filopodia [1, 5, 6]. Viruses require host cell processes to maximize replication and spread. Several clinically significant viruses, including influenza virus, HIV-1, and SARS-CoV-2, were shown to exploit intercellular tunneling nanotubes (TNTs) to move their genome to naive cells and bypass host immunity [7–10]. TNTs are F-actin–based tubular structures several hundred microns long that connect 2 homo- or heterologous cells, providing continuity of plasma membrane and cytoplasm between the connected cells. This allows the cells to rapidly exchange components, including proteins, RNA, and organelles (eg, mitochondria and endosomes) [11, 12]. Because the transport speed through TNTs is rapid, it would be energetically more favorable for a virus to traffic the genome intercellularly to propagate infection, in contrast to undergoing the conventional replication cycle. Additionally, viral genome transfer by TNTs would broaden the host cell tropism, further contributing to disease development, and it would facilitate virus persistence in the host, effectively avoiding host immune defenses and countermeasures [7]. Understanding how viruses exploit TNTs during infection is therefore key to designing more effective treatments. Herein, we investigated the involvement of TNTs in EBOV intercellular dissemination.
EBOV proteins and RNA localize to TNTs during infection. MΦs infected with EBOV at MOI = 1 for 48 hours were stained with phalloidin, RedDot2 dye (blue), and either (A) antibodies to VP40 and GP or (B) antibody to NP and a probe binding NP RNA. Samples were analyzed as in Figure 1B. The solid arrowheads point to TNTs positive for all tested viral factors. The hollow arrowhead points to a TNT containing only VP40. EBOV, Ebola virus; GP, glycoprotein; MOI, multiplicity of infection; NP, nucleoprotein; TNT, tunneling nanotube.Marija A Djurkovic, Carson G Leavitt, Eusondia Arnett, Valeriia Kriachun, Luis Martínez-Sobrido, Rossella Titone, Laura J Sherwood, Andrew Hayhurst, Larry S Schlesinger, Olena Shtanko
Ebola Virus Uses Tunneling Nanotubes as an Alternate Route of Dissemination
The Journal of Infectious Diseases, Volume 228, Issue Supplement_7, 15 November 2023, Pages S522–S535, https://doi.org/10.1093/infdis/jiad400
Copyright: © 2023 The authors.
Published by Oxford University Press on behalf of Infectious Diseases Society of America. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
And even if, as creationists also insist, 'Sin' is to blame for pathogens, there is the small problem of the nanotubules between cells which makes the virus safe from our immune system as it infects more cells. Presumably no creationist would claim these were also designed by 'Sin' since they are an essential part of the structure and function of tissues. Did the omnipotent, omniscient designer not anticipate that it would be used to keep pathological viruses safe from the immune system it designed to protect us, so they can kill us more easily?
So many problems for creationists, all so they can avoid accepting that a simpler explanation is that this is all the result of a mindless natural evolutionary process with no gods, good bad or indifferent, involved.
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