How it spreads - According to the NHA, WHA and various health commissions and organizations, the virus originated from central Fusea. The flu quickly spreaded around the continent, most notably, Paxiosolange. As you may know, Paxiosolang Olympic athletes have transmitted the virus to Franshov - eventually contaminating the Olympic Park... The pathogen spreads through physical contact, water droplets, (coughing, sneezing) and travels its way into the stomach. As it does, it moves around the body and damaging the immune system... making the victim vunerable. Physical contact with anyone who is thought to be sick, is not be advised.
Source: Toshavo Breaking New Issue 8190

GIV transmission has been updated; the disease can be transmitted by droplets (coughing, sneezing, bleeding, salivating), skin contact, and now livestock
Source: Dispatch from the Jon Fred Sr. Medical and Biological Research Centre, Paxiosolange

The GIV virus is:

• Terminal (Non-cured)
• Contagious via skin contact
• Contagious via droplets (i.e coughing, sneezing)
• Gateway to other afflictions (hepatitis, skin-cancer, flu, pox)

Source: Doctor Jon Fred Jr.

However while the GIV-1 exhibits many characteristics of influenza it more closely resembles the HIV virus as it targets cells from the immune system, nulling the bodies natural immune response to the infection.

HIV
When someone is exposed to an HIV virus (through infection) their immune system is targeted particularly the helper T cell. The HIV virus attacks the helper T-cell, infects and then kills the cell to spread the virus. Without the function of the T cell other immune cells such as B- cells cannot function to make antibodies which in turn cripples the immune system.

(1) The human immunodeficiency virus (HIV) particle (top) travels through the bloodstream and (2) attaches to the receptor on the surface of a lymphocyte (bottom), an immune system cell involved in fighting infections. (3) Genetic material (RNA) from the virus enters the lymphocyte and, (4) with the help of an enzyme called reverse transcriptase, makes copies of itself to be inserted into the genetic material of the host lymphocyte. (5) Copies of the virus' genetic material are inserted into the genetic material of the lymphocyte. (6) This new genetic material in the cell causes the lymphocyte to make the "blueprint" needed for manufacturing new HIV particles. This blueprint contains the code for making virus proteins. An enzyme known as a protease acts to clip the large virus protein molecules into smaller pieces so they can be used to make new HIV particles. (7,8) New HIV particles are produced and released from the lymphocyte, which is destroyed. These viruses can then travel through the body and enter and destroy other cells.

The GIV-1 and Macrophages
For the GIV-1 virus to become such an effective pathogen it has both characteristics of the influenza virus as well as the HIV virus and used the human bodies immune response to accelerate the spreading of the disease. For this to occur the GIV-1 has been observed passively luring T cells with its coating of hemagglutinin a protein used to bind the virus to cell membranes typically found in the lungs. However the main function of the virus is to "Hijack" macrophages. The virus accomplishes this by allowing B cells to digests antigen hemagglutinin to pass onto helper T-cells which activate allowing macrophages to target the GIV-1. When the macrophages attack the GIV-1 they engulf the virus and begin to break it down using enzymes from its lysosomes, however this triggers the release of Genetic material (RNA) from the virus which then enters the lymphocyte and with the help of an enzyme called reverse transcriptase, makes copies of itself to be inserted into the genetic material of the host lymphocyte. Copies of the virus' genetic material are inserted into the genetic material of the lymphocyte. This new genetic material in the cell causes the lymphocyte to make the "blueprint" needed for manufacturing new HIV particles. This blueprint contains the code for making virus proteins. There is also a secondary effect of the GIV-1 in which it instructions the infected macrophage (IM) to attack the cells of the host body. During these attacks the IM engage in the destruction of healthy tissue which it begins to break down though phagocytosis. Instead of ejecting cell material as waste the new "blueprints" instruct the IM to construct new GIV-1 viruses to be released back into the body, further targeting more macrophages continuing the attack on the body.

GIV-1 enters the body primarily through the respiratory system as well as absorption through other bodily membranes. It then attaches to host cells. Its antigen protein coating is detected by Beta cells which trigger a response to T-cells which activate macrophages to terminate the GIV-1. When the GIV-1 is engulfed by the macrophage the process of phagocytosis breaks the protein layer surrounding the GIV-1 releasing the nucleocapsid containing the genetic material of the GIV-1 into the macrophage. With the help of an enzyme called reverse transcriptase, the virus makes copies of itself to be inserted into the genetic material of the host lymphocyte. It produces instructions that alter the host macrophage and changes the macrophages protein recognition. The macrophage has become and IM and begins attacking healthy cells in the body, breaking down molecules to be made into new GIV-1 viruses that are released from the IM. As the cycle continues, the increase number of IMs in the body call for increase response from T-cells that release more macrophages into the body that are then infected by newly produced GIV-1 viruses. Cytokine is also released by the T-cells which excessively increases inflammation leading to further tissue damage and eventual death of the host.