a. Higher order taxa
Viruses do not have a domain, phylum or class. Thus, the taxa begins at order. Porcine circovirus is classified as follows:
Viruses; ssDNA viruses; Circoviridae; Circovirus; unclassified Circovirus
2. Description and significance
Circoviruses are small ssDNA viruses which can inhabit and infect several hosts. Porcine circoviruses commonly infect swine (2). There are two main serotypes: Porcine circovirus 1 (PCV1) and Porcine circovirus 2 (PCV2). There is current research into another emerging serotype, Porcine circovirus 3 (PCV3), which is very similar to PCV2, but is not yet an epidemic in swine (13). PCV1 is not known to demonstrate any sign of disease, whereas PCV2 can cause an illness called Porcine circovirus Associated Disease (PCVAD), which causes Post Weaning Multisystemic Wasting Syndrome (PMWS) (3, 4). Porcine circovirus has one of the highest evolution rates of DNA viruses and also has the capability to co-infecting hosts along with other pathogens. This can lead to more severe outbreaks and complex syndromes involving reproductive failure, enteritis and pneumonia (5).
The Porcine circovirus has the smallest genome of any autonomously replicating virus (5). The small size of the genome presents many challenges when attempting to study the pathology of the virus in livestock. The circovirus can affect a variety of hosts (mostly livestock); moreover, Porcine circovirus infection can have detrimental effects on agricultural business as it can kill off an entire swine herd, and hence cut into profits (6). Infection results in a high fatality rate in swine populations, even though a vaccine has been created to protect against PMWS. The circovirus’ small genome allows for fast evolutionary adaption, permitting the virus to quickly gain resistance to these vaccines (5, 7). This is due to the fact that one or two mutations could have a huge effect on the virus, such as making a benign circovirus pathogenic (3).
3. Genome structure
The Porcine circovirus has two major serotypes, type 1 and type 2 (PCV1 and PCV2) and one emerging serotype, type 3 (PCV3) (13). PCV1 is known to be benign, while PCV2 is pathogenic (3, 4). Porcine circovirus 2 (PCV2) is a small, non-enveloped virus with a circular single-stranded DNA genome which is 1.76kb (6, 8). Since the genome of circovirus is small it also allows for more recombination events with other similar viruses. For example, it has been shown historically through phylogenetic analysis that a nanovirus and a circovirus at some point recombined, as a circovirus has some RNA segments in its genome even though it is a ssDNA virus (2). The DNA sequence similarity between the two serotypes, PCV1 and PCV2, is about 76% (9).
4. Cell structure
Porcine circovirus has a diameter of around 17 nm, thus making it the smallest animal virus studied with the capability of independent replication (8). Porcine circovirus is a non-enveloped virus assembled by a single capsid.
5. Metabolic processes
Viruses do not have their own metabolism, but instead take advantage of their host cells to replicate, transcribe, and translate. The PCV genome enters the host cell nucleus by inserting into daughter nuclei at the end of mitosis (10). The two proteins Rep and Rep’ are the replication initiator of ORF (Open Reading Frame) C1 transcript, which code for the capsid protein for porcine circovirus (10).
Porcine circovirus 2 (PCV2) is highly infectious to swine. Studies determined that Porcine circovirus is a derivative of a former swine virus. The genome of the microbe and the cap (capsid) sequences of PCV2a and PCV2b viral genomes were aligned to determine any possible location of recombination in the sequence (11). Furthermore, circoviruses have been coevolving with many different vertebrate organisms for millions of years (2, 11). In fact, the current evolutionary model of the Porcine circovirus is as follows: PCV2 is a virus that has long been associated with swine, and only recently has become infectious (11).
Evidence shows that Porcine circovirus acts as an immunosuppressive agent which can open up the host to a secondary infection (3). It can lead to the development of Porcine circovirus-associated diseases (PCVAD) which are connected to many varying swine diseases (6). The most common disease that develops, within swine, is Post Weaning Multisystemic Wasting Syndrome (PMWS). PMWS is commonly found in swine 6-8 weeks with enlarged lymph nodes, jaundice, and extreme loss of weight (3). Some swine show symptoms of respiratory distress and interstitial pneumonia (3). PMWS has a high fatality rate with infected swine. To prevent this disease vaccines and prevention strategies for PCV2a were developed. Prevention strategies included monitoring the health of weaning swine, avoid having a high density of swine together, and control the movement of swine between batches (3). This however has caused the evolution of the virus to serotype PCV2b in swine populations, thus reducing the potential for prevention (6, 7). Porcine circovirus is not a zoonotic agent, and therefore there is little concern for possible infection to humans (12).
Porcine circovirus is a global disease. In the United States and Italy, PCV3 was isolated and identified in 2015 (13). Researchers are currently working to reduce the rate of infection of PCV3 with epidemiological analysis of the virus. Ultimately, epidemiologists hope the virus will not spread as quickly as PCV2 and will therefore avoid becoming an epidemic in swine populations around the globe. As of 2017 Italy was the only EU country with PCV3 which seemed to have similar genetic properties to the virus found in the US (13).
8. Current Research
Include information about how this microbe (or related microbes) are currently being studied and for what purpose
It is required that you add at least five primary research articles (in same format as the sample reference below) that corresponds to the info that you added to this page. [Sample reference] Faller, A., and Schleifer, K. "Modified Oxidase and Benzidine Tests for Separation of Staphylococci from Micrococci". Journal of Clinical Microbiology. 1981. Volume 13. p. 1031-1035.