en.wikipedia.org/wiki/Andes_virus

This sentence is outdated and misleading. Modern primary-source evidence identifies protocadherin-1 (PCDH1) as the key cell-entry receptor for Andes virus (ANDV) and other New World/American orthohantaviruses.

A 2018 Nature paper reported that PCDH1 is an essential determinant of entry and infection for both Andes virus (ANDV) and Sin Nombre virus (SNV), and that the viral glycoproteins directly recognize PCDH1 for entry. The same study also showed that genetic ablation of PCDH1 made hamsters highly resistant to lethal ANDV challenge.

The current ICTV genus report for Orthohantavirus is consistent with that result: in its lifecycle description, it states that after engaging a cellular receptor, "protocadherin 1 in the case of American orthohantaviruses" mediates entry. Andes virus is an American orthohantavirus.

Older literature did propose β3 integrins as receptor candidates or attachment factors, so this wording likely reflects superseded literature. But stating flatly that ANDV enters cells "by using β3-integrins as receptors" is not accurate given the later receptor-identification work and current ICTV description.

This sentence conflicts with current structural descriptions of orthohantavirus surface spikes in two ways.

1. The spikes are not described as having helical symmetry. The ICTV report describes orthohantavirus envelopes as having square-shaped spikes made of tetrameric Gn-Gc heterodimers that form a surface lattice with local symmetry. Structural papers likewise describe the hantaviral spike as a tetrameric (Gn-Gc)4 assembly.

2. The sentence reverses the head/stalk arrangement of Gn and Gc. Structural studies place the Gn head domain (GnH) at the membrane-distal/head region of the spike, where it shields the fusion loops of Gc. In other words, Gn is part of the outer/head region, not simply the stalk with Gc forming the head.

So the article's wording is inaccurate both in calling the spike symmetry "helical" and in assigning Gn to the stalk and Gc to the head.

The sentence reverses the role of cap snatching in hantavirus transcription.

For hantaviruses, the viral polymerase uses short capped fragments stolen from host mRNAs as primers for viral mRNA synthesis. In other words, cap snatching is part of initiating and generating viral mRNA, not a later step that occurs only after the genome has already been transcribed.

The ICTV family report states that hantavirus proteins are produced from capped viral mRNAs and that the 5′ cap structure is obtained via cap snatching from cellular mRNAs. The ICTV Orthohantavirus report further notes that the L protein mediates cap-snatching for viral mRNA capping and that during transcription, host-cell-derived capped primers are used. A PNAS paper on hantavirus cap snatching likewise states that these viruses initiate viral transcription through cap snatching and that the capped RNAs are used by the viral polymerase during transcription initiation.

So the problem is the article's sequence of events: cap snatching is not something RdRp does only after transcription to make an already-transcribed RNA translatable; it is part of how the viral mRNA is generated in the first place.