Question: What allows the viral genome RNA to spread to other cells?
About the article "RNA", section "RNA genomes".

Candidate passages:
Poliovirus is a natural neuropathogen, making it the obvious choice for selective replication in tumours derived from neuronal cells.
Poliovirus has a plus-strand RNA genome, the translation of which depends on a tissue-specific internal ribosome entry site (IRES) within the 5' untranslated region of the viral genome, which is active in cells of neuronal origin and allows translation of the viral genome without a 5’ cap.
Gromeier et al.
(2000) replaced the normal poliovirus IRES with a rhinovirus IRES, altering tissue specificity.
The resulting "PV1(RIPO)" virus was able to selectively destroy malignant glioma cells, while leaving normal neuronal cells untouched. 
Viruses can replicate only in living cells.
Influenza infection and replication is a multi-step process: First, the virus has to bind to and enter the cell, then deliver its genome to a site where it can produce new copies of viral proteins and RNA, assemble these components into new viral particles, and, last, exit the host cell.
Influenza viruses bind through hemagglutinin onto sialic acid sugars on the surfaces of epithelial cells, typically in the nose, throat, and lungs of mammals, and intestines of birds (Stage 1 in infection figure).
After the hemagglutinin is cleaved by a protease, the cell imports the virus by endocytosis.
The intracellular details are still being elucidated.
It is known that virions converge to the microtubule organizing center, interact with acidic endosomes and finally enter the target endosomes for genome release.
Once inside the cell, the acidic conditions in the endosome cause two events to happen: First, part of the hemagglutinin protein fuses the viral envelope with the vacuole's membrane, then the M2 ion channel allows protons to move through the viral envelope and acidify the core of the virus, which causes the core to dissemble and release the viral RNA and core proteins.
The viral RNA (vRNA) molecules, accessory proteins and RNA-dependent RNA polymerase are then released into the cytoplasm (Stage 2).
The M2 ion channel is blocked by amantadine drugs, preventing infection.
These core proteins and vRNA form a complex that is transported into the cell nucleus, where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense vRNA (Steps 3a and b).
The vRNA either is exported into the cytoplasm and translated (step 4) or remains in the nucleus.
Newly synthesized viral proteins are either secreted through the Golgi apparatus onto the cell surface (in the case of neuraminidase and hemagglutinin, step 5b) or transported back into the nucleus to bind vRNA and form new viral genome particles (step 5a).
Other viral proteins have multiple actions in the host cell, including degrading cellular mRNA and using the released nucleotides for vRNA synthesis and also inhibiting translation of host-cell mRNAs.
Negative-sense vRNAs that form the genomes of future viruses, RNA-dependent RNA polymerase, and other viral proteins are assembled into a virion.
Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane.
The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion (step 6).
The mature virus buds off from the cell in a sphere of host phospholipid membrane, acquiring hemagglutinin and neuraminidase with this membrane coat (step 7).
As before, the viruses adhere to the cell through hemagglutinin; the mature viruses detach once their neuraminidase has cleaved sialic acid residues from the host cell.
After the release of new influenza viruses, the host cell dies.
Because of the absence of RNA proofreading enzymes, the RNA-dependent RNA polymerase that copies the viral genome makes an error roughly every 10 thousand nucleotides, which is the approximate length of the influenza vRNA.
Hence, the majority of newly manufactured influenza viruses are mutants; this causes antigenic drift, which is a slow change in the antigens on the viral surface over time.
The separation of the genome into eight separate segments of vRNA allows mixing or reassortment of vRNAs if more than one type of influenza virus infects a single cell.
The resulting rapid change in viral genetics produces antigenic shifts, which are sudden changes from one antigen to another.
These sudden large changes allow the virus to infect new host species and quickly overcome protective immunity.
This is important in the emergence of pandemics, as discussed below in the section on Epidemiology. 
The assembly of infectious coronavirus particles requires the selection of viral genomic RNA from a cellular pool that contains an abundant excess of non-viral and viral RNAs.
Among the seven to ten specific viral mRNAs synthesized in virus-infected cells, only the full-length genomic RNA is packaged efficiently into coronavirus particles.
Studies have revealed cis-acting elements and trans-acting viral factors involved in coronavirus genome encapsidation and packaging.
Understanding the molecular mechanisms of genome selection and packaging is critical for developing antiviral strategies and viral expression vectors based on the coronavirus genome. 
 genomes.
Like DNA, RNA can carry genetic information.
RNA viruses have genomes composed of RNA that encodes a number of proteins.
The viral genome is replicated by some of those proteins, while other proteins protect the genome as the virus particle moves to a new host cell.
Viroids are another group of pathogens, but they consist only of RNA, do not encode any protein and are replicated by a host plant cell's polymerase.
Influenza type A viruses are very similar in structure to influenza viruses types B and C. The virus particle (also called the virion) is 80–120 nanometers in diameter and usually roughly spherical, although some rare filamentous forms can occur.
According to researchers, there are more filamentous particles in clinical isolates, whereas laboratory strains consist of more spherical virions.
Despite these varied shapes, the virions of all influenza type A viruses are similar in composition.
They are all made up of a viral envelope containing two main types of proteins, wrapped around a central core.
The two large proteins found on the outside of viral particles are hemagglutinin (HA) and neuraminidase (NA).
HA is a protein that mediates binding of the virion to target cells and entry of the viral genome into the target cell, while NA is involved in the release of progeny virions from infected cells.
These proteins are usually the targets for antiviral drugs.
Furthermore, they are also the antigen proteins to which a host’s antibodies can bind and trigger an immune response.
Influenza type A viruses are categorized into subtypes based on the type of these two proteins on the surface of the viral envelope.
There are 16 subtypes of HA and 9 subtypes of NA known, but only H 1, 2 and 3, and N 1 and 2 are commonly found in humans.
The central core of a virion contains the viral genome and other viral proteins that package and protect the genetic material.
Unlike the genomes of most organisms (including humans, animals, plants, and bacteria) which are made up of double-stranded DNA, many viral genomes are made up of a different, single-stranded nucleic acid called RNA.
Unusually for a virus, though, the influenza type A virus genome is not a single piece of RNA; instead, it consists of segmented pieces of negative-sense RNA, each piece containing either one or two genes which code for a gene product (protein).
The term negative-sense RNA just implies that the RNA genome cannot be translated into protein directly; it must first be transcribed to positive-sense RNA before it can be translated into protein products.
The segmented nature of the genome allows for the exchange of entire genes between different viral strains.
The entire Influenza A virus genome is 13,588 bases long and is contained on eight RNA segments that code for 11 proteins:  Segment 1 encodes for HA (hemagglutinin).
About 500 molecules of hemagglutinin are needed to make one virion.
HA determines the extent and severity of a viral infection in a host organism.
Segment 2 encodes NA (neuraminidase).
About 100 molecules of neuraminidase are needed to make one virion.
Segment 3 encodes NP, which is a nucleoprotein.
Segment 4 encodes two matrix proteins (M1 and M2) by using different reading frames from the same RNA segment.
About 3000 matrix protein molecules are needed to make one virion.
Segment 5 encodes two distinct non-structural proteins (NS1 and NEP) by using different reading frames from the same RNA segment.
Segment 6 encodes an RNA polymerase (PA); an alternate form of this polymerase can sometimes be made with a change to the reading frame  Segment 7 encodes another RNA polymerase (PB1) and the PB1-F2 protein, which induces cell death, by using different reading frames from the same RNA segment   Segment 8 encodes a third RNA polymerase (PB2).
The RNA segments of the viral genome have complementary base sequences at the terminal ends, allowing them to bond to each other with hydrogen bonds.
After transcription from negative-sense to positive-sense RNA takes place, the positive-sense RNA strands are capped on the 5’ end by a process called cap snatching.
This involves the viral protein NS1 binding to the host cell’s early messenger RNA transcripts.
A second viral protein, PA, cleaves the cap from the host’s RNA.
The short cap is then added to the influenza positive-sense RNA strands, allowing it to be processed by ribosomes and translated into its protein products.
The positive-sense RNA strands also serve for synthesis of negative-sense RNA strands for new virions.
The RNA synthesis takes place in the cell nucleus, while the synthesis of proteins takes place in the cytoplasm.
Once the viral proteins are assembled into virions, the assembled virions leave the nucleus and migrate towards the cell membrane.
The host cell membrane has patches of viral transmembrane proteins (HA, NA, and M2) and an underlying layer of the M1 protein which assist the assembled virions to budding through the membrane, releasing finished enveloped viruses into the extracellular fluid.