Viral Spread Model

[insert screenshot of the simulation] Cauliflower mosaic virus (CaMV) is typically spread from plant to plant through aphids acting as viral vectors. Once in the plant cell, CaMV exploits host transport mechanisms in order to spread. Neighbouring plant cells share cytoplasmic connections through connections called plasmodesmata, which are utilized by CaMV to spread to neighbouring cells. Additionally, viruses can also form tubules through cell walls to spread to adjacent cells. These two processes, however, are quite slow. An additional feature of the plant that the virus able to exploit is the plant’s vascular system, where it is able to spread quickly through the plant’s vascular system, leading to what is called systemic infection. [insert diagram of the plant’s plasmodesmata and vascular system] As a reaction to the presence of the virus, the plant cells will destroy infected cells through apoptosis as well as signal to the rest of the plant to begin production of defensive chemicals in preparation for attack. This signaling causes systemic required resistance, a broad, long-term increased resistant to future infections. (Ryals et al., 1994) -Explain and link this to the parameters in the model once the parameters are finalized -Explain reasons for the parameters

Plant Structure

Virus

Plant Response

Biological Background

Viral Spread Mechanisms

Intercellular

Cauliflower mosaic virus exploits host transport mechanisms in order to spread. Neighbouring plant cells share cytoplasmic connections through connections called plasmodesmata. These symplastic connections are exploited by CaMV to spread to neighbouring cells, but it is a fairly slow process. The virions must travel between the plasma membrane and the desmotubule (cytoplasmic channel) of the plasmodesmata, a very narrow passage. The size of molecule able to diffuse through the plasmodesmata is determined by the size exclusion limit (SEL), which is affected by the gating properties of the plasmodesmata. In another slow cell-to-cell process, the virus can move through tubules formed through the cell wall. However, CaMV is able to spread to different regions of the plant quite quickly using the plant’s phloem (sugar-transport network). Microtubules are a key component of intercellular transmission as well as intracellular motion. They form viral inclusions that encourage uptake by aphids (the major plant-to-plant transport agent) and of viral factories (Niehl et al., 2013). CaMV can induce the formation of microtubules in order to increase its rate of spread .

Systemic Infection

-Phloem/Vascular System

Plant Defense Mechanisms

Hypersensitive Response (HR)

Systemic Acquired Resistance (SAR)

Mechanisms

The systemic acquired resistance (SAR) defense mechanism, or immunization of plants, is a broad, long-term increased resistant to future infections. (Ryals et al., 1994) This is similar to the increased resistance against diseases in mammals, after having been infected. (Ryals et al., 1994) It is important to note that this resistance is not triggered by mechanical damage caused by factors such as herbivore attack. (Ryals et al., 1994) This mechanism is only activated after a pathogen is detected within the plant, triggering defenses through signals (Ryals et al., 1994) Salicylic acid (SA) has been identified as a molecule with an indispensable role in the pathway to systemic acquired resistance. (Klessig et al., 2000) Additionally, NO also has an important role in activating systemic acquired resistance. (Klessig et al., 2000) During the initial wave of defense after pathogen detection, there is an “oxidative burst” wherein levels of oxidative species suddenly increase. (Klessig et al., 2000) This is accompanied by cell wall protein linkage, the activation of kinase and increased gene expression defensive genes. (Klessig et al., 2000) A second wave of defense is found in the hypersensitive response, wherein lesions form (from programmed cell death). (Klessig et al., 2000) NO and SA play an interconnected role with each other, where reactive oxygen species (ROS) such as NO have been observed accumulating SA, and in turn, SA triggers ROS production (including NO and H2O2). (Klessig et al., 2000)

Signalling and Spread

Software Choices

Originally, three different agent-based modelling (ABM) software packages (MASON, MESA and Netlogo) were chosen out of several as the top candidates to create the viral spread simulation. All of the languages required for the simulation packages were unfamiliar to the team, and thus would have to be learned from scratch. Netlogo was chosen to create the final simulation due to a variety of its strengths as well as time constraints. Although Netlogo was the most unfamiliar-looking language, it presented itself as the simulation package with the smallest learning curve. Additionally, it had readily-available documentation and a built-in GUI. MESA was a Python-based simulation package and ultimately was not chosen due to its documentation not being as detailed or as readily available as MASON or Netlogo’s, as well as the level of familiarity with Python required to create the model being too high to achieve within the time constraints. MASON, a Java-based simulation package, despite having excellent, easily-found documentation did not have a built-in GUI, and did not have as many built in-functions as the Netlogo, thus requiring more work to get off the ground. Although in some cases the fewer amount of built-in functions could have proved to be an advantage (it would have added more flexibility and customization to the simulation), due to the time constraints and the demand of a level familiarity with Java (as with MESA) to create a simulation with MASON, Netlogo was thus chosen over MASON.