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I took a look at the lytic cycle on wikipedia. Every fact which requires some form of prior knowledge is referenced with a primary or secondary research article. There doesn't seem to be any direct phrasing and everything referenced has been rephrased from the original statement. However, there are some citations missing, there are some claims made which do not have citations to back them up.

The article stays on topic and does not deviate from the original idea. It is well written and accessory information is not given.

The article is nor persuasive. It is written in a very neutral manner and does not try to convince the reader of anything. It just states the facts and allows you to formulate your own opinion. This paper does not seem to have a biased.

The sources used in the article seem to biased. This fact is not stated anywhere in the article, which is a problem.

The early and late phases of the lytic cycle seem to be under represented. Even though there are many different possible pathways, they could have given one as an example. Everything else is explained thoroughly.

Their replication have two dominant cycles: lytic and temperate cycles. Viral nucleic acid replication and synthesis of virus encoded protein is considered as the lytic cycle. However, a bacterium infected by a temperate or dormant phage is called the temperate cycle [1]. To meet metabolic demand of replication, viruses recruit a multitude of strategies to sequester nutrients from their host. One such technique is to starve their host cell. This is done by inhibiting the host cells CO2 fixation, which enables the cyanophage to recruit photosynethically formed redox and ATP from the host cell to meet their nucleotide and metabolic response [2]. Cyanophage’s contain genes known as viral-encoded auxiliary metabolic genes (AMGs), which encode critical, rate-limiting steps of the host organism [2]. AMGs encode genes for the pentose phosphate pathway, phosphate acquisition, sulfur metabolism, and DNA/RNA processing; these genes interfere with the metabolism of the host cell. Metagenomic analysis highly supports the notion that these genes promote viral replication through the degradation of host DNA and RNA, as well as a shift in host cell metabolism to nucleotide biosynthesis [2]. Cyanophages also use these genes to maintain host photosynthesis through the progression of the infection, shuttling the energy away from carbon fixation to anabolism, which the virus takes advantage of [3]. AMGs genes also code for proteins, which aid in the repair of the host photosystem, which is susceptible to photodegredation [3]. One such example are the D1 proteins which replace the host cells D1 protein when it becomes damaged [3]. The virus up-regulates photosynthesis, which leads to an increased rate of D1 protein degradation, the host cell alone can not efficiently replace these proteins so the cyanophage replaces them for the host cell so it can continue to provide energy for the cyanophage replication cycle [3].

            It is evident that cyanophage replication is heavily dependent on the diel cycle. The first step in the infectious cycle is for the cyanophage to make contact and bind to the cyanobacteria, this adsorption process is heavily dependent on light intensity[4]. Field studies also show that the infection and replication of cyanophages is directly or indirectly synchronized with the light-dark cycle [4]

Marine cyanophages of the family Myoviridae help regulate primary production mainly through infection of Synechococcus spp.[5]. The other two families, Podoviridae and Siphoviridae, are usually found in freshwater ecosystems [5]. In coastal oceans, abundance can reach >106 mL-1 and are also found in sediments.

The viruses cannot move independently and must rely on currents, mixing, and host cells to transport them. They cannot actively target their hosts and must wait to encounter them. This may explain why Myoviridae primarily infect one of the most abundant cyanobacteria, Synechoccocus, because the probability of collision is higher . Evidence of co-variation between the phages and hosts, in addition to an increase in cyanophages above 103 to 104 Synechococcus mL-1, suggest a “kill-the-winner” regulation dynamic . Synechococcus contribute 25% of all photosynthetic biomass in the ocean, having significant bottom-up effect on higher trophic levels[6]. The dissolved organic matter (DOM) released from viral lysis of cyanophages can be shunted into the microbial loop where it is recycled or some of it rejected by heterotrophic bacteria to form recalcitrant matter that is eventually buried in sediment[6]. This is an important step in atmospheric carbon sequestration, commonly referred to as the biological pump, and maintenance of other biogeochemical cycles[6].

Cyanobacteria perform oxygenic photosynthesis which is thought to be the origin of atmospheric oxygen approximately 2.5Ga ago[7]. Population, and therefore, rate of oxygen evolution can be regulated by cyanophages. In certain species of cyanobacteria such as Trichodesmium that perform nitrogen fixation, cyanophages are capable of decreasing the rate of inorganic nitrogen conversion to bioavailable organic nitrogen[8][9].

Cyanophages control blue-green algae blooms that can be toxic to human health and cause eutrophication, leading to oxygen minimum zones. Cyanophages can infect and kill four common bloom-forming cyanobacteria: Lyngbya birgei, Anabaena circinalis, Anabaena flosaquae, and Microcystis aeruginosa [1].

Blooms cause problems ecologically, economically, and in freshwater systems, quality of drinking water[10] . Spikes in cyanobacteria populations are usually brought on by nutrient increase due to upwelling of remineralized waters or run-off from fertilizers, dust, and sewage[11]

By killing hosts, the Myoviridae help restore the ecosystem to its natural balance.

In addition to regulating population size, cyanophages likely influence phylogenetic composition [11]. Due to the lysogenic phase of their replication cycle, cyanophages may behave as mobile genetic elements for genetic diversification of their hosts through horizontal gene transfer[12][13]. Whether the lytic or lysogenic phase dominates in a given area has been hypothesized to depend on eutrophic or oligotrophic conditions, respectively [14].

Increase in number of encounters is directly related to an increase in rate of infection providing more opportunity for selective pressure, making coastal Synechococcus more resistant to viral infection [5].

File:T4 virus infects bacteria adhesion.gif
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  1. ^ a b Jassim, Sabah A. A.; Limoges, Richard G. (2013-10-01). "Impact of external forces on cyanophage–host interactions in aquatic ecosystems". World Journal of Microbiology and Biotechnology. 29 (10): 1751–1762. doi:10.1007/s11274-013-1358-5. ISSN 0959-3993.
  2. ^ a b c Kaplan, Aaron (2016). "Cyanophages: Starving the Host to Recruit Resources". Cell. 26: R511–R513 – via Science Direct.
  3. ^ a b c d Frank, Jeremy A.; Lorimer, Don; Youle, Merry; Witte, Pam; Craig, Tim; Abendroth, Jan; Rohwer, Forest; Edwards, Robert A.; Segall, Anca M. (2013-06-01). "Structure and function of a cyanophage-encoded peptide deformylase". The ISME Journal. 7 (6): 1150–1160. doi:10.1038/ismej.2013.4. ISSN 1751-7362. PMC 3660681. PMID 23407310.{{cite journal}}: CS1 maint: PMC format (link)
  4. ^ a b Ni, Tianchi; Zeng, Qinglu (2016-01-01). "Diel Infection of Cyanobacteria by Cyanophages". Frontiers in Marine Science. 2. doi:10.3389/fmars.2015.00123. ISSN 2296-7745.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ a b c Suttle, Curtis A. (2000-01-01). Whitton, Brian A.; Potts, Malcolm (eds.). The Ecology of Cyanobacteria. Springer Netherlands. pp. 563–589. doi:10.1007/0-306-46855-7_20. ISBN 9780792347354.
  6. ^ a b c Wang, Kui; Wommack, K. Eric; Chen, Feng (2011-11-01). "Abundance and Distribution of Synechococcus spp. and Cyanophages in the Chesapeake Bay". Applied and Environmental Microbiology. 77 (21): 7459–7468. doi:10.1128/AEM.00267-11. ISSN 0099-2240. PMC 3209163. PMID 21821760.{{cite journal}}: CS1 maint: PMC format (link)
  7. ^ Schirrmeister, Bettina E.; Antonelli, Alexandre; Bagheri, Homayoun C. (2011-01-01). "The origin of multicellularity in cyanobacteria". BMC Evolutionary Biology. 11: 45. doi:10.1186/1471-2148-11-45. ISSN 1471-2148. PMC 3271361. PMID 21320320.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  8. ^ Bergman, Birgitta; Sandh, Gustaf; Lin, Senjie; Larsson, John; Carpenter, Edward J. (2013-05-01). "Trichodesmium– a widespread marine cyanobacterium with unusual nitrogen fixation properties". FEMS Microbiology Reviews. 37 (3): 286–302. doi:10.1111/j.1574-6976.2012.00352.x. ISSN 0168-6445. PMC 3655545. PMID 22928644.{{cite journal}}: CS1 maint: PMC format (link)
  9. ^ Kashyap, A. K.; Rai, A. N.; Singh, Surendra (1988-06-01). "Effect of cyanophage N-1 development on nitrogen metabolism of cyanobacterium Nostoc muscorum". FEMS Microbiology Letters. 51 (2–3): 145–148. doi:10.1111/j.1574-6968.1988.tb02986.x. ISSN 0378-1097.
  10. ^ Beversdorf, Lucas J.; Miller, Todd R.; McMahon, Katherine D. (2013-02-06). "The Role of Nitrogen Fixation in Cyanobacterial Bloom Toxicity in a Temperate, Eutrophic Lake". PLOS ONE. 8 (2): e56103. doi:10.1371/journal.pone.0056103. ISSN 1932-6203. PMC 3566065. PMID 23405255.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  11. ^ a b Fuhrman, Jed (1993). "VIRUSES SYSTEMS IN MARINE PLANKTONIC" (PDF). Oceanography. 6: 51–63.
  12. ^ Frost, Laura S.; Leplae, Raphael; Summers, Anne O.; Toussaint, Ariane. "Mobile genetic elements: the agents of open source evolution". Nature Reviews Microbiology. 3 (9): 722–732. doi:10.1038/nrmicro1235.
  13. ^ Jassim, Sabah A. A.; Limoges, Richard G. (2013-10-01). "Impact of external forces on cyanophage–host interactions in aquatic ecosystems". World Journal of Microbiology and Biotechnology. 29 (10): 1751–1762. doi:10.1007/s11274-013-1358-5. ISSN 0959-3993.
  14. ^ Weinbauer, Markus (2011). "Virus-Mediated Redistribution and Partitioning of Carbon in the Global Oceans": 54–56 – via Research Gate. {{cite journal}}: Cite journal requires |journal= (help)
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