No one claims that we're descended from viruses, and most commentators don't even give the viruses credit for being 'alive', but it seems clear that they are distant relatives and that we share much of the same genomic machinery.   


Viruses (Wiki) 
http://en.wikipedia.org/wiki/Virus#Origins 
Long, very informative article with many links. 

Regressive hypothesis 

Viruses may have once been small cells that parasitised larger cells. Over time, genes not required by their parasitism were lost. The bacteria rickettsia and chlamydia are living cells that, like viruses, can reproduce only inside host cells. They lend support to this hypothesis, as their dependence on parasitism is likely to have caused the loss of genes that enabled them to survive outside a cell. This is also called the degeneracy hypothesis.^[36][37]

Cellular origin hypothesis

Some viruses may have evolved from bits of DNA or RNA that "escaped" from the genes of a larger organism. The escaped DNA could have come from plasmids (pieces of naked DNA that can move between cells) or transposons (molecules of DNA that replicate and move around to different positions within the genes of the cell).^[38] Once called "jumping genes", transposons are examples of mobile genetic elements and could be the origin of some viruses. They were discovered in maize by Barbara McClintock in 1950.^[39] This is sometimes called the vagrancy hypothesis.^[36][40]

Coevolution hypothesis

Viruses may have evolved from complex molecules of protein and nucleic acid at the same time as cells first appeared on earth and would have been dependent on cellular life for many millions of years. Viroids are molecules of RNA that are not classified as viruses because they lack a protein coat. However, they have characteristics that are common to several viruses and are often called subviral agents.^[41] Viroids are important pathogens of plants.^[42] They do not code for proteins but interact with the host cell and use the host machinery for their replication.^[43] The hepatitis delta virus of humans has an RNA genome similar to viroids but has protein coat derived from hepatitis B virus and cannot produce one of its own. It is therefore a defective virus and cannot replicate without the help of hepatitis B virus.^[44] Similarly, the virophage 'sputnik' is dependent on mimivirus, which infects the protozoan Acanthamoeba castellanii.^[45] These viruses that are dependent on the presence of other virus species in the host cell are called satellites and may represent evolutionary intermediates of viroids and viruses.^[46][47]

Prions are infectious protein molecules that do not contain DNA or RNA.^[48] They cause an infection in sheep called scrapie and cattle bovine spongiform encephalopathy ("mad cow" disease). In humans they cause kuru and Creutzfeldt-Jakob disease.^[49] They are able to replicate because some proteins can exist in two different shapes and the prion changes the normal shape of a host protein into the prion shape. This starts a chain reaction where each prion protein converts many host proteins into more prions, and these new prions then go on to convert even more protein into prions. Although they are fundamentally different from viruses and viroids, their discovery gives credence to the idea that viruses could have evolved from self-replicating molecules.^[50]." 

I was very surprised to discover that some virus genomes include the code for producing G protein-coupled receptors.  Searching PubMed for "virus G protein-coupled receptors" yielded 5,709 articles.  Some of them are below. 


1993   
Virally encoded G protein-coupled receptors: targets for potentially innovative anti-viral drug development.. (PubMed) 
http://www.ncbi.nlm.nih.gov/pubmed/?term=12816350
Abstract only.   
    Further confirmation, but still no explanation.   
    "Various herpes- and poxviruses contain DNA sequences encoding proteins ... which belong to the family of G protein-coupled receptors (GPCRs) ... Cytomegalovirus (CMV) ... encodes four GPCRs." 


1998   
G-protein-coupled receptor of Kaposi's sarcoma-associated herpesvirus is a viral oncogene and angiogenesis activator. (PubMed)     
http://www.ncbi.nlm.nih.gov/pubmed/?term=9422510   
Abstract only.   
    "G-protein-coupled receptor encoded by an open reading frame (ORF 74) of KSHV".  If I understand correctly, this seems to mean that the virus includes the genetic code for a GPCR.  ???? The abstract makes no attempt to explain how this might be possible. 


2001   
Virally encoded 7TM receptors (PubMed)   
http://www.nature.com/onc/journal/v20/n13/abs/1204191a.html 
Full length article and a partial explanation.   
    "A number of herpes- and poxviruses encode 7TM G-protein coupled receptors most of which clearly are derived from their host chemokine system as well as induce high expression of certain 7TM receptors in the infected cells." 
    "... viruses have adopted host genes and structurally optimized their products for particular pharmacological phenotypes to benefit the virus. Thus, certain members of the large DNA virus families, i.e. the Herpesviridae and the Poxviridae have incorporated chemokines and/or chemokine receptors from their hosts into their own viral genome ..."  


2004   
Insights into the viral G protein-coupled receptor encoded by human herpesvirus type 8 (HHV-8) (PubMed)   
http://www.ncbi.nlm.nih.gov/pubmed/?term=15207903
Abstract only. 
    This confirms that the virus does, indeed, encode the GPCR.   
    "HHV-8-GPCR is a chemokine-like receptor encoded by KSHV, the etiologic agent of KS."  There was a lot of this that I didn't understand.  "In in vitro systems, HHV-8-GPCR signals via multiple transduction pathways including, activation of phospholipase C and PKC, inhibition of adenylyl cyclase, activation of nuclear factor-kappaB; activation PI 3-kinase, p42/44 MAPK and Akt/PKB, and activation of JNK/SAPK, p38 MAPK and RAFTK. HHV-8-GPCR is important in the HHV-8 life cycle because HHV-8-GPCR-deficient viruses do not replicate in response to chemokines and exhibit, less efficient reactivation from latency." 


2008 
The virophage as a unique parasite of the giant mimivirus.  (PubMed) 
Only abstract available online. 
    "Viruses are obligate parasites of Eukarya, Archaea and Bacteria. Acanthamoeba polyphaga mimivirus (APMV) is the largest known virus; it grows only in amoeba and is visible under the optical microscope. Mimivirus possesses a 1,185-kilobase double-stranded linear chromosome whose coding capacity is greater than that of numerous bacteria and archaea."  


2009   
The origin of viruses. (PubMed) 
Only abstract available online. 
    "Viruses are parasitic organisms that live in infected cells and produce virions to disseminate their genes. Most viral proteins have no homologues in modern cells, in contradiction with the traditional view of viruses as pickpockets of cellular genes. This suggests that viral genes essentially originated in the virosphere during replication of viral genomes and/or were recruited from cellular lineages now extinct. Some specific viral proteins are present in viruses infecting members of the three domains of Life, suggesting that viruses are indeed very ancient. In particular, structural analyses of capsid proteins have revealed that at least two types of virions originated independently before the LUCA (the Last Universal Cellular Ancestor). Although several hypotheses have been recently proposed to explain the origin of viruses, the emergence of virions, as a specific mechanism for gene dissemination, remains unexplained."  


2009 
On the origin of cells and viruses: primordial virus world scenario. (PubMed) 

    "All the uncertainties involved notwithstanding, it seems to be extremely likely that LUCA was fairly complex, that is, had at least about as many genes as the simplest of the modern free-living prokaryotes, namely, on the order of a 1000 genes or more. Figures in this range have been inferred by all algorithmic methods for ancestral gene set reconstruction ^{5, 11, 12, 19}. However, given the uncertainty associated with these approaches (see above), the more compelling argument for a complex LUCA is the complexity is of the modern translation machinery that comprises indisputable LUCA heritage. The functioning of such an advanced translation system is predicated on commensurate metabolic capabilities including not only the pathways for the synthesis of all nucleotides and (nearly) all amino acids but also those for at least some coenzymes, e.g., S-adenosylmethionine, the cofactor of the numerous RNA methylases several of which can be traced back to LUCA with a high confidence ^{18, 34}. Furthermore, the evolutionary relationships of some translation system components imply that these proteins are products of preceding complex evolution. A case in point are the aminoacyl-tRNA synthetases (aaRS), the 20 enzymes (one for each amino acid) that are essential for translation and of which, at least, 18 are confidently traced back to LUCA ^{35, 36}. The core catalytic domains of the aaRS represent two distinct classes that possess unrelated structural folds and cover 10 amino acid specificities each. Analysis of the evolutionary history of the catalytic domains of Class I aaRS indicates that they all comprise one cluster of terminal branches in the elaborate tree of the “Rossmann-like” protein domains ^{37, 38}. Thus, the diversification of the aaRS, that was already (nearly) complete in LUCA, was preceded by complex protein evolution including the divergence of many families of enzymes. The same argument applies to translation factors, RNA methylases, and other groups of proteins involved in translation ₁₈. Logically, these observations clinch the case for a LUCA whose genetic complexity was, in the least, not much lower than that of simple modern prokaryotes."  
     "Russell and coworkers proposed that networks of microcompartments that exist at both extant and ancient hydrothermal vents, and consist, primarily, of iron sulfide could be ideal habitats for early life. These inorganic compartment networks provide gradients of temperature and pH that could fuel primordial energetics, and versatile catalytic surfaces for primitive biochemistry 55, 56. These might have been the sites of prebiological and pre-cellular biological evolution, from mixtures of organic molecules to the putative, primordial RNA world to the independent escapes of archaeal and bacterial cells 23, 45. These compartments are envisaged being inhabited by diverse populations of genetic elements, initially, segments of RNA, subsequently, larger and more complex RNA molecules encompassing one or a few protein-coding genes, and later yet, also DNA segments of gradually increasing size (Fig. 3). Notably, a computer simulation study has shown that, in the presence of thermal gradient that inevitably exists at a hydrothermal vent, extremely high concentrations of small molecules and polymers can be reached 57, a condition that would substantially facilitate a variety of reactions including RNA ligation 58.

Figure 3 
The primordial virus world model of pre-cellular evolution   
    - Click to enlarge - 

    Thus, early life forms, likely including LUCA, are perceived as complex ensembles of genetic elements that inhabited networks of inorganic compartments ^{45, 59}. A key feature of this model is that genetic elements with different replication and expression strategies (including replicating DNA segments) encoding distinct replication machineries would coexist within a network or even within the same compartment. " 

    See:  Montmorillonite . 


2009   
The great billion-year war between ribosome- and capsid-encoding organisms (cells and viruses) as the major source of evolutionary novelties.     
    Abstract: http://onlinelibrary.wiley.com/enhanced/doi/10.1111/j.1749-6632.2009.04993.x 
    "After the discovery of mutations and the cracking of the genetic code, it was usually believed that mutations (originally mostly envisaged as single mutations) were the main sources of variation. More recently, it became evident that more complex processes are at work. Brosius wrote recently, focusing on retroviruses and eukaryotic cells, that “the interaction of hosts with retroviruses, retrotransposons and retroelements is one of the eternal conflicts that drive the evolution of life.”³¹ We would like to extent this argument here to the whole biosphere by postulating that, once viruses appeared on the stage of life, the major cause of variation became the interplay between viral and cellular genomes, and the major cause of selection became the war between capsid and ribosome-encoding organisms. We thus finally conclude that the billion years war between cells and viruses has been (and still is) the major engine of life evolution."  


2010   
DNA Viruses: The Really Big Ones (Giruses)  (PubMed)  
Full length HTML and PDF available online for free.   
    "The polydnaviruses are enigmatic with respect to genes and particle structure, means of replication, and transmission (see sidebar, Polydnaviruses); these are not considered further. Other large, dsDNA-containing viruses have genomes ranging from 100 to 280 kb, including herpesviruses, asfarviruses, baculoviruses, iridoviruses, and ascoviruses, and also are not discussed in this review.