Reo Viruses:

Respiratory Enteric Orphan (REO) viruses infect human respiratory system and intestinal tracts; they don’t manifest any symptoms that is why ,they are called orphan viruses i.e. they are in search of a disease.  But now it is known that they do cause diseases such as infantile Diarrhea and Colorado tick fever and others.  There are more than 150 species; they infect animals and plants as well. They include Rotavirus.

Aqua Reo virus; http://www.colgate.edu/

One more diagram of Reovirus depicting various structural features; http://www.microbiologybytes.com/

Genus:	Outer capsid:	Core:	Non-structural:
Reoviruses:	σ-1, σ-3, μ-1c, λ-2	λ-1, λ-3, σ-2, μ-2	μ-NS, σ-NS
Orbiviruses:	VP2, VP5, VP7	VP3; VP1,VP4,VP6 (transcriptase complex)	NS1, NS2, NS3
Rotaviruses:	VP4, VP7	VP2, VP6, VP1, VP3	NSP1, NSP2, NSP3, NSP4, NSP5, NSP5A

Microbiology bytes ; http://www.microbiologybytes.com/

General features:

All have isometric shape, naked, 70 to 85 nm thick, and made up of two concentric capsid layers.

• Genomic RNA exists as double stranded structures, ten different segments; each coding for a specific protein.

• Replicating enzymes are found within the core of the viruses.

• At the vertices, it has sigma 1HA proteins for cell recognition.  On the inner surface of the inner coat, nonstructural proteins are found which are associated with ds RNA genomes, which are ten in number.

Viral Proteins:

Gene/protein	Mol.wt (KD)	Function
Lambda-1	155	Inner capsid (core protein)
Lambda-2	140	Inner core-Guanyl transferase
Lambda-3	140	Replicase
Micron 1C	80	Outer capsid protein
Micron 2	72-80	Inner core
Micron NS1	80	Nonstructural protein
Micron NS2	36	Nonstructural protein
Sigma 1	42	Spike, 1HA
Sigma 2	38	Inner capsid protein
Sigma 3	34	Outer capsid protein

Replication:

Entry is gained through the spike protein binding to cellular receptors, and endocytosis leads to endosomes. 

· Inside endosomes outer capsid digested to release inner core, which now becomes active.

This figure shows the infection and reproductive cycle of the virus;

Development of Oncolytic Reovirus for Cancer Therapy; Ergin Sahin; http://file.scirp.org/

There are 10-(11?) dsRNA genomes, each code one or more proteins,

· The RNA dependent RNA polymerase or what is called RNA Replicase start replicating to produce only positive sense RNA from all the ten segments, as each transcript represents one protein. 

· What is not clear, but speculated, whether or not the ds RNA fully formed RNAs or one of them especially (+) strand is incomplete, at the time of infection.

· Aftermath of infection and activation, the incomplete plus strands of RNA are completed and the same are released into cytoplasm.  The released (+) RNAs have cap structure at 5’ end with out a poly (A) tail.

· The negative RNA strands also have pppG-Pu-Py sequences at the 5’ end.  The plus sense RNAs, as they are synthesized, they come out of the pores found at vertices.   It is through the pores in the capsid, all the required NTPs and other components for replication enter. Even the RNA strands synthesized inside the viral capsid move out.

· Synthesis and the release of (+) RNAs continue.  The (+) RNA transcripts in cytoplasm act as mRNAs and they associate with ribosomes and translate.

· As sufficient number of the inner capsid proteins and replicating enzymes are produced, they get assembled into provirus particles with all ten different species of (+) RNAs. 

· Within these core particles, plus RNAs are transcribed or say replicated to generate (-) RNAs.  Pro- viral particles continue to produce more (+) RNAs and more proteins and more (-) RNAs. 

· As process goes on, many pro-viral cores with ds RNAs get encapsulated with second coat proteins to produce new viral particles. 

Many of the mechanisms are not well understood (or I haven’t got the material to know about it?).