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u/ManyCryptographer316

ANDES Paradox solved: Why this virus mutated & still is the same like 2018
▲ 1 r/hantavirus

ANDES Paradox solved: Why this virus mutated & still is the same like 2018

Hi,

the "controversial" member of this subreddit is here, joining you with utmost confidence. Observing how this subreddit reacts to different information is kinda cool to see.

So to end the discussions here afterall:

- this outbreaks Clade 3 strain has mutated. It has mutated to become more infectious then previous Clade 3.

- surprise: It has mutated in the same way that Clade 2 did. It has literally two mutations that Clade 2 in 2018 had when it had a "super-spreader" event.

- surprise: This indeed very likely changes pH dependent entry towards 6.37 for this outbreaks Clade 3 strain. This makes it likely more likely to fuse to your cells in your upper airways and eyes.

- for people not understanding: 2018 we already had these same mutations in another Clade 2. Now this outbreak's Clade 3 strain experienced what we call convergent evolution.

- the HVAC and humidity did play an enormous role in this outbreak and because of that I predict: most of the flight passengers sitting not directly beside but +1 rows away from the infected will be tested negative

- there will be limited Gen 3 spread. We will not see a pandemic with this.

- common flu medication works against the virus in vitro. So..

...here is something we should be more concerned about:

Everyones personal mental health.

reddit.com
u/ManyCryptographer316 — 4 days ago
▲ 56 r/hantavirus

ANDV Hantavirus: A summary on what we know (Strain, Transmission, Mutations, Genetics, Treatments & Protections)

As there is much confusion about the virus, misinformation spread everywhere, media outlets are still not covering this, people calling fear & calm mongering:
Let me summarize it for you, so you can make educated life choices:

It's the ANDV Clade 3 stray
Switzerland/Hu-3337/2026 is within the ANDV Clade 3 Cluster. Historically, Clade 3 was not involved in H2H transmissions. It was rodent to human only. This outbreak is a very subnormal phenotypic shift. This strain just unlocked (super-)spreading capabilities which were previously only seen in Clade 2 strains (2018 birthday outbreak).

Transmission happens through Aerosols
Every news outlet reporting "close contact required" is lying. Evidence like neighboring cabins getting infected without direct H2H contact as well as certain mutations (see next section) are highly suggesting that the virus is able to transmit vi Aerosols. Joseph Allen (Harvard) model suggests Hu-3337/2026 is able to stay in humid air for up to 2 hours. We think that the HVAC on the MV Hondius did not include cabin HEPA filters and recirculated air, acting as an "aggregator" concentrating the viral mist from cabin to cabin.
We have to check cases in Argentina and Chile for H2H transmissions through sequencing the genoms of infected persons from there. This can make or break the humid air hypothesis, or even give evidence about potential arid air potential. We currently think that transmission is mainly fueled in this region due to high prevalence of rats in cities due to wildfires and previous weather conditions that lead to overpopulation of rats.

The strain mutated – Synonymous SNPs in L-segments (C2139T, G576A) + mutation in Gc fusion loop
According to an analysis of the virus is under pervasive negative selection (roughly 73% codons), meaning it has a sweet spot that it is not likely to mutate away from (coding mutations are unlikely). Non-coding mutations happened, as they don't effect core protein structural changes. SNPs in L-segment C2139T and G576A are the "fingerprint" of the current outbreak on Hondius. Mechanistic models are suggesting that these changes or the mutations in GC fusion loop act as replication multiplications. They may shift the pH trigger higher (to 6.2), which would facilitate faster entry (45mins->15mins) and give it the ability to efficiently start replication in the upper respiratory tract. To give you context: A similar situation happened for Delta->Omicron in COVID19. We currently think that Hu-3337/2026 (current Honidus strain that was sequenced) could because of this change in replication behavior be already infectious before symptoms start. We have still to sequence more people's infections from the cruise ship and their contacts to understand dynamics. Reproduction currently outpaces genomic sequencing.

Analysis of susceptibility and protection

  • ITGB3 > rs5918 (L33P): CC genotype is highly protective. TT genotype (Leucine) was found in majority (ca. 90%) of infected humans.
  • PCDH1: This is used by the virus strain to enter the human body. It is found on the eyes, nose, lungs, etc. Thus you have to wear air-tight eye protection, we think, to protect yourself from infectious aerosols.
  • Genetic variations in EC1 domain, specifically F83L residue 83 determine cell susceptibility, as they alter virus's ability to key endothelial receptors.
  • HLA-B*35, Outcome marker:
    • HLA-B*35:05 and
    • HLA-B*35:08 markers are found exclusivly in patients with mild clinical course. Other variants are linked to severe outcomes.
  • We know that IGg antibodies stay behind for a longer period of time after infection, giving some immunity to people.

Anything to reduce infection risk?

  • Encounter Barriers like Nitric Oxide (NO) nasal sprays block receptor binding, CPC and Lactoferrin lozenges act as surfactants.
  • If in high risk scenarios, due to changed behavior of virus, you can reduce risk by spraying NO directly before and after risk exposure.
  • During exposure use CPC / Lactoferrin lozenges and Lactoferrin nasal spray and eye drops.
  • Generally: Zink 25mg / day + Lactoferrin OTC supplement (likely to reduce risk for severe infection).
  • If in non-hotspots & socially feasible, Air tight eye-protection, FFP2/3 masks also are essential.
  • If in hotspots: Wear protective gear.

No supplement replaces the need for a fit-tested respirator in areas with active Clade 3 transmission.

Do we have any treatments?
In Chile, cleaned plasma of previously infected people is used to reduce mortality rate to below 15%. We also have some drugs that might work:

  • Favipiravir reduces viral polymerase, inhibiting replication, efficacy shown in animal models.
  • Baloxavir acid (used against common cold viruses) are shown in vitro to reduce replication drastically, suspected efficacy equal to Favipiravir.
  • Ribavirin (only severe cases due to side effects). Molnupiravir (or Galidesivir) could (maybe) help (mutagenic nucleotide) reducing replication stability, but Baloxacir acid is 100-1000x more active in vitro.
  • Lactoferrin inhibits entry, together with Ribavirin in studies it lead to high inhibiton of viral loads. It is available OTC. Inhances resilience, primes interferons. Known immunomodulator.
  • Nafamostat and Camostat could block pH-dependent entry.

Surfaces & Desinfectants: Surfactants are and probably will be able to work, as the virus is adhering to it's structural proteins. It's a encapsulated virus, meaning unstability, which is good for surfactants.

What do do now:
Monitor cases until June 10th (if there are second & third waves with mutated strain and how many cases). Await Hamburgs reverse genetics for a functional analysis.

I will keep this post updated every couple of days, if I see major developments.

Cheers.

Sources:
https://virological.org/t/preliminary-analysis-of-orthohantavirus-andesense-virus-sequences-from-a-cruise-ship-related-cluster-may-2026/1029
https://virological.org/t/complete-sequence-of-orthohantavirus-andesense-virus-swiss-resident-2026/1023
https://www.biorxiv.org/content/10.64898/2026.03.17.712151v1.full
https://www.researchgate.net/publication/14285599_Hantaviruses_Genome_structure_expression_and_evolution
https://pmc.ncbi.nlm.nih.gov/articles/PMC4661284/
https://www.news-medical.net/news/20260227/New-structural-insights-pave-way-for-hantavirus-vaccines.aspx
... and some more.

u/ManyCryptographer316 — 8 days ago