Friday 26 July 2024

Malevonet Designer News - How Herpes Uses Sneak Tactics To Infect More People


Skin blisters caused by herpes zoster (shingles)
Suppression of the host antiviral response by non-infectious varicella zoster virus extracellular vesicles | Journal of Virology

If you're going to design pathogens to overcome the immune system and make people sick, it helps that you know the weaknesses of the immune system you designed earlier to protect people from the pathogens you design.

To devotees of creationism's divine malevolence, the sheer brilliance of its designs is breathtaking, but the question they always avoid is why did it design the immune system with so many flaws and weak points in the first place? Was that merely incompetence, or did it intend to exploit them.

The redness of the rash may not be apparent on black or brown skin.
Creationists also carefully avoid questions about why any intelligent designer would have these arms races with itself, like someone with multiple personality syndrome and amnesia who constantly forgets what it designed yesterday and designs a new solution to the same problem today, and who sees the solutions to problems it designed yesterday as new problems to be solved today.

This is the supposed designer that creationists call 'intelligent', and which they would rather people believe in than have them accept the materialist explanation - mindless evolution proceeding without a plan in which one organism with its strengths and weaknesses is merely part of another organism's environment, presenting opportunities and threats, and selectors which pushes the population of organisms in a direction which makes them better fitted to survive and produce the next generation.

Rash around the eyes can be painful and may affect sight and hearing.
Alas, the excuses creationists try to make for this appearance of incompetent stupidity in design that parasites provide us with when we look below the superficial - genetic entropy and the ludicrous notion of 'devolution' - is demonstrably nonsensical, since an advantageous mutation can't logically be described as 'devolutionary' or somehow less perfect than its predecessor without private definitions of the words, 'perfect' and 'better' to mean the exact opposite of what normal people mean by them.

The latest example of a parasite appearing to be designed to increase the suffering in the world by sneaking past the incompetently designed immune system, if you believe in the childish 'intelligent design' notion, is the way the herpes virus that causes chicken pox and shingles manages to spread throughout the body where it lies dormant until something like illness, old age or infirmity triggers it to reactivate an cause shingles.

Tell me all about the varicella zoster virus, please. The varicella-zoster virus (VZV) is a highly contagious virus belonging to the herpesvirus family, specifically known as Human herpesvirus 3 (HHV-3). It is responsible for causing two distinct diseases: chickenpox (varicella) and shingles (herpes zoster). Here’s a detailed overview of VZV:

Structure and Transmission
  • Structure: VZV is an enveloped virus with a double-stranded DNA genome. It has an icosahedral capsid surrounded by a lipid envelope that contains viral glycoproteins essential for infection.
  • Transmission: The virus spreads primarily through respiratory droplets when an infected person coughs or sneezes, and by direct contact with the fluid from chickenpox or shingles blisters.

Varicella (Chickenpox)
  • Symptoms: Chickenpox is characterized by an itchy, blister-like rash that appears first on the chest, back, and face and then spreads over the entire body. Other symptoms include fever, fatigue, and headache.
  • Incubation Period: The incubation period is typically 10-21 days after exposure to the virus.
  • Complications: While generally mild in children, chickenpox can cause severe complications such as pneumonia, encephalitis, and bacterial infections of the skin in adults and immunocompromised individuals.
  • Prevention: The varicella vaccine is highly effective in preventing chickenpox. It is recommended for children, adolescents, and adults who have not had chickenpox.

Herpes Zoster (Shingles)
  • Reactivation: After a person recovers from chickenpox, VZV remains dormant in the nerve tissues. It can reactivate years later as shingles, particularly in older adults and those with weakened immune systems.
  • Symptoms: Shingles causes a painful rash that typically appears on one side of the body or face, following the path of a nerve. Other symptoms include pain, burning, or tingling in the affected area, fever, and headache.
  • Complications: Complications can include postherpetic neuralgia (chronic pain in the areas where the shingles rash occurred), vision loss if the eyes are affected, and neurological problems if the central nervous system is involved.
  • Prevention: The shingles vaccine (such as Shingrix) is recommended for older adults to prevent reactivation of the virus.

Diagnosis and Treatment
  • Diagnosis: VZV infections are usually diagnosed based on clinical symptoms. Laboratory tests, such as polymerase chain reaction (PCR), direct fluorescent antibody (DFA) testing, or viral culture, can confirm the diagnosis.
  • Treatment: - For chickenpox, treatment primarily involves symptom relief, such as antihistamines for itching and acetaminophen for fever. Antiviral medications like acyclovir may be prescribed for high-risk individuals. - For shingles, antiviral drugs (acyclovir, valacyclovir, or famciclovir) are most effective when started early in the course of the disease. Pain management may include analgesics, corticosteroids, or nerve pain medications.

Public Health Impact
  • Vaccination Programs: The introduction of the varicella vaccine has significantly reduced the incidence of chickenpox and its associated complications. Vaccination has also decreased the incidence of shingles in vaccinated populations by reducing the overall circulation of VZV.
  • Surveillance: Public health organizations monitor VZV infections to control outbreaks and assess the effectiveness of vaccination programs.

Research and Developments
  • Ongoing research aims to improve vaccines, develop new antiviral treatments, and understand the mechanisms of VZV latency and reactivation. Understanding the virus's interaction with the host immune system is crucial for developing better preventive and therapeutic strategies.

In summary, the varicella-zoster virus is a significant human pathogen with a major impact on public health. Vaccination remains the most effective measure to prevent both primary infection and reactivation of the virus.
The varicella zoster virus (VZV) rapidly produces a battery of small extracellular vesicles (sEVs) that penetrate the cells in distant parts of the body. These sEVs contain a protein which shuts down the cells immune response, making them vulnerable to infection by the virus as it spreads along neurons to other tissues.

In effect, the virus sends a squad of fifth columnists into the body to sabotage the defences, like an invading army, making a takeover easy with little or no resistance. If that had been intelligently designed, you would have to admire the designer - that is, until you realised that the same designer was also responsible for designing the defences. This is no surprise for biologists, since we know from the Theory of Evolution that the 'designer' is not a single sentient entity but a mindless, unintelligent process working without a plan.

This mechanism was discovered by a team of researchers at the University of Colorado's Anschutz Medical Campus who have reported their findings in the Journal of Virology. It is described in a University of Colorado Anschutz Medical Campus news release:
Scientists Identify Key Protein Behind Spread of Shingles Virus
For the first time, researchers identify the mechanism that allows the varicella zoster virus to spread far from the infection site

Scientists at the University of Colorado Anschutz Medical Campus have discovered a new evasion strategy used by the varicella zoster virus, which causes chickenpox and shingles, which may allow it to affect tissues far from the original site of infection.
The study was published today in the Journal of Virology.

The researchers, using human neurons and rodent models, honed in on a single viral protein known as IE62 that is packaged and shuttled throughout the body in structures known as small extracellular vesicles (sEVs). They discovered that IE62 packaged inside sEVs can travel from the site of infection, where it penetrates cells and shuts down their antiviral response, opening the door to infection by the virus.

The virus, known as VZV, is ancient and common, residing within 95% of all people. Its primary infection causes chickenpox, which then goes latent. During stress, aging, or other factors, VZV can reactivate into shingles, a painful skin disease that can also attack the central nervous system and can lead to vascular disease, stroke, dementia, and other serious conditions.

To rapidly spread throughout the body, the virus needs an immediate strategy to evade the immune system. This study is the first to show exactly how it does this by exploiting the infected cells sEV machinery.

This is the first time a clear mechanism has been found that actually ties this virus to an avenue by which it can affect distal organs, far from the site of infection. These vesicles shut down the immune response.

Assistant Professor Dr. Christy Niemeyer, PhD, first author
University of Colorado Anschutz Medical Campus
Aurora, Colorado, USA.



The study’s senior author Andrew Bubak, PhD, assistant professor of neurology at the CU School of Medicine, said the protein shuts down the anti-viral response in the cells far sooner than previously known.

We believe this protein is likely being packaged into sEVs and shuttled down the neurons that go to your skin, making the cells under the skin vulnerable to the whole infection. We think this precedes the rash, which is obviously interesting from a therapeutic standpoint.

This mechanism can offer us clues into how other viruses work and cause infection.

Assistant Professor Dr. Andrew N. Bubak, PhD, senior author
Department of Neurology
University of Colorado Anschutz Medical Campus
Aurora, Colorado, USA.


While there is a vaccine for shingles, there are currently no drugs to impact the activity of this protein. That could change.

This study is the first to identify a different anti-viral target that perhaps we can develop therapeutics for. We need to better understand their role in viral spread and secondary disease development to reduce the systemic complications caused by VZV infections.

Assistant Professor Dr. Christy Niemeyer, PhD.


Bubak said this mechanism may be responsible for the prevalent co-infections and immunosuppressive events seen clinically in those infected with VZV. He also noted that the virus can intermittently reactivate in individuals without the classic shingles rash, evading diagnosis and raising the question of whether this immunosuppressive event occurs more frequently than originally thought.

Niemeyer agreed, saying the significance of sEVs in the spread of this virus highlights the need for further investigation.

ABSTRACT
Varicella zoster virus (VZV) reactivates from ganglionic sensory neurons to produce herpes zoster (shingles) in a unilateral dermatomal distribution, typically in the thoracic region. Reactivation not only heightens the risk of stroke and other neurological complications but also increases susceptibility to co-infections with various viral and bacterial pathogens at sites distant from the original infection. The mechanism by which VZV results in complications remote from the initial foci remains unclear. Small extracellular vesicles (sEVs) are membranous signaling structures that can deliver proteins and nucleic acids to modify the function of distal cells and tissues during normal physiological conditions. Although viruses have been documented to exploit the sEV machinery to propagate infection, the role of non-infectious sEVs released from VZV-infected neurons in viral spread and disease has not been studied. Using multi-omic approaches, we characterized the content of sEVs released from VZV-infected human sensory neurons (VZV sEVs). One viral protein was detected (immediate-early 62), as well as numerous immunosuppressive and vascular disease-associated host proteins and miRNAs that were absent in sEVs from uninfected neurons. Notably, VZV sEVs are non-infectious yet transcriptionally altered primary human cells, suppressing the antiviral type 1 interferon response and promoting neuroinvasion of a secondary pathogen in vivo. These results challenge our understanding of VZV infection, proposing that the virus may contribute to distant pathologies through non-infectious sEVs beyond the primary infection site. Furthermore, this study provides a previously undescribed immune-evasion mechanism induced by VZV that highlights the significance of non-infectious sEVs in early VZV pathogenesis.

IMPORTANCE
Varicella zoster virus (VZV) is a ubiquitous human virus that predominantly spreads by direct cell-cell contact and requires efficient and immediate host immune evasion strategies to spread. The mechanisms of immune evasion prior to virion entry have not been fully elucidated and represent a critical gap in our complete understanding of VZV pathogenesis. This study describes a previously unreported antiviral evasion strategy employed by VZV through the exploitation of the infected host cell’s small extracellular vesicle (sEV) machinery. These findings suggest that non-infectious VZV sEVs could travel throughout the body, affecting cells remote from the site of infection and challenging the current understanding of VZV clinical disease, which has focused on local effects and direct infection. The significance of these sEVs in early VZV pathogenesis highlights the importance of further investigating their role in viral spread and secondary disease development to reduce systemic complications following VZV infections.

Again, what we see when we look beyond the superficial are examples of incompetence and abundant examples of malevolence, if you accept the childish intelligent [sic] design notion. A moment’s thought, with minimal understanding of biology, will expose the daft notions of 'genetic entropy' and 'devolution', invented to get around the embarrassment that parasites and arms races causes creationism, as sciencey-sounding gibberish, designed to appeal to the scientifically illiterate and hard of thinking creation cult.



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1 comment :

  1. Chickenpox and Shingles are serious diseases. Creationists invoke The Fall or Original Sin of Adam and Eve, which is a load of dung. That's just a myth written by ignorant people and its so vague and ambiguous its impossible to interpret. There's so much it doesn't address and it raises so many questions and doesn't answer any of them. The Bible just causes confusion. There's not much clarity in the Bible which is one reason why so many different Churches, denominations, interpretations, and different Bible translations exist. There's not much of anything Christians agree on. Christians are among the most confused, divided, and splintered people in the world. The Bible is vague, ambiguous, unclear, and filled with so many contradictions its a huge embarrassment. How could such a sloppily written book be the inspired infallible word of God?
    It's wise to get vaccinated. Life is an endless struggle and battle against germs and diseases. The creator is a cruel, sadistic, insane, demented, malevolent, amoral, mentally blind, morally blind bastard who has no conscience. Kindness and healing diseases is up to us humans and not some God. God has no clue what kindness is.

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