1.1 The Lyssasangravirus

1.1.1 General

The lyssasangrevirus, or 'bloody rage' is believed to be a strain of the lyssavirus, or rabies virus. It is a zoonotic, neuroinvasive virus in that mammals are the only viable carriers and specifically targets the neural cells of the host. It is named as such due to the hosts aggression and profuse bleeding from minor injuries.

1.1.2 Transmission

Due to high quantities of the virus existing in the salivary glands coupled with the hosts aggressive behaviour, bite causing an open wound is the primary method of transmission.

Transmission may also occur from blood contact and fluid transfer such as ingestion/absorption of fluids expelled from the infected patient, e.g. vomit. Continuous grabbing and scatching motions causing jagged fingernails surrounded by torn tissue can cause infection if a scratch breaks the epidermis.

1.1.3 Stage 1 - Infection [24h]

Similar to the rabies, or lyssavirus, on infection the virus travels the neural pathways to the brain. The time to reach the central nervous system is generally short, averaging 6 hours. The bloodstream carries the virus to other parts of the body where it targets neural tissue.

Few symptoms evident other that a influenza-like increase in mucus production. The patient generally feels unwell.

1.1.4 Stage 2 - Propagation [36h]

Once reaching the brain, the virus binds with neural cells and reproduces rapidly. A response of the hypothalamus is to produce moderate quantities of an anticoagulant. Patients may begin to notice greater than normal blood loss from typical wounds.

Motor nerves are bound to and are strengthened by the virus in that the cell membranes are hardened. Sensory nerves when attached begin to deteriorate and act as sites of strong further propagation. Infection of the nerves causes symptoms ranging from numbness and/or irritation to intense pain, and involuntary movement or 'twitching'.

Encephalytis causes fever, headaches, hyperphagia, confusion and aggression. Some loss of controlled motor function may occur.

1.1.5 Stage 3 - Final [48h]

The virus has bound with most cells of the brain. Senses such as taste and smell will be significantly diminished, with affected hearing and eyesight.

The virus RNA binding with the cerebellum and frontal lobes creates a crude symbiotic relationship, in that the cell structure is maintained so long as the cell contains adenosinetriphosphate. This in effect gives the host minimal logic ability to focus electrical impulses across hardened motor neurons, specifically low motor skills. Smaller areas of behaviour are also maintained, specifically maintaining the primary emotion of the host. Patients have been known to attack in aggression or scream fearfully until death.

Intermittent impulses causing muscle spasms are evident in the host, specifically in the heart and lungs producing an audible moaning sound and light ejections of blood and fluid from wounds.

Severe loss of motor function. The patient may have limited ability to walk and will attempt to grab at other mammals, human or otherwise, with little to no accurate motor skills.

Most other lobes of the brain are functional only as sites of reproduction, and are eventually destroyed. This results in complete loss of short and long term memory.

Normal bodily functions will cease and clinical death results.

In some cases the involuntary movement has continued for hours after death, and occasionally the host has made voluntary movements and eye contact for short periods after death, indicating some level of cognition exists as a result of the virally maintained neural tissues. Presumably a lack of ATP quickly occurs and the cells die.

1.2 The Halinespirovirus

1.2.1 General

The halinespirovirus, 'life of no breath' virus is a satellite virus, in that it cannot reproduce without co-infection with a master virus. The pathogen is known to have co-infected with the influenza virus. Patients are often seen to survive in either a comatose or seriously brain damaged state for several hours before clinical death, despite having significantly desecrated dermis and organ failure.

1.2.2 Transmission

The virus depends on transmission methods of the host virus, as it specifically (and unusually) attaches to the host virus.

1.2.3 Stage 1 - Infection [30h]

The virus is carried across the host via the bloodstream and specifically binds with muscle tissue cells where it will begin to reproduce rapidly. The patient will begin to feel sore muscles.

1.2.4 Stage 2 - Propagation [40h]

The virus rapidly reproduces with little to no effect on the host pathogen. The host cells begin to produce significant levels of a cytotoxic acid causing proteolysis. Fat deposits will be depleted first. Muscles will retain structure and function, drawing energy from the anaerobic processes. The stomach lining acts as a sieve pulling protein from stomach contents.

The host will begin to experience moderate to intense pain across the body, especially at the primary site of infection.

The bodily response to the anaebolic respiration will be a form of intense hunger and the host will crave specifically protein rich foods.

Other symptoms may possibly include, but are not limited to intense nausea/vomiting, blueish tinge to skin due to internal bruising, and weakness.

1.1.5 Stage 3 - Final [50h]

The onset of chronic anaemia causes the patient to suffer severe lethargy and agonal respiration. If the brain has been infected severe damage due to cerebral hypoxia results, with general psychosis and coma.

The digestive system will shut down. The osmotic behaviour of the stomach lining causes continual deterioration of the stomach contents, which become toxic after several hours.

Necrosis will begin in depleted cells, particularly in skin and organ tissue. Due to the rapid nature of this process the host experiences severe pain if conscious. The host will stop breathing at approximately 45 hours, but due to increased anaerobic process some level of brain and muscle function continue for several hours. If conscious, the host will either be in a state of intense fear, shock or intense psychosis. Some hosts have been known to maintain eye contact and even move for a short period afterwards.

At approximately 50 hours the host will experience brain dysfunction and clinical death.

2.1 General

The most fearsome coupling of virii seen since HIV and tuberculosis in first millenia Europe, the co-infection of lyssasangre and halinespiro virii causes a host to become intensely hungry for protein rich sustenance, visibly decay over time and actually remain mobile after the cardio-pulmonary system has ceased to function. Receptors in the body and brain are disabled so the host feels no sensations, yet the eyes and ears remain functional. The phase period is of the disease is significantly shortened due to the host's inability to combat two level 4 pathogens.

2.2 Transmission

See 1.1.2

2.3 Stage 1 - Infection [12-15h]

The host will experience a range of symptoms including nausea, influenza-like symptoms and significant pain at the primary site of infection. See 1.1.3 and 1.2.3

A host can die before 3 hours and the lyssasangre and halinespiro virus will not continue to propagate provided the former has not reached the cerebellum. In some cases infection may occur if the virus has entered the host in close proximity to the brain or brain stem, such as a bite to the head or sternamastoid region of the neck. The lyssasangrevirus will cause the host to sustain the brain long enough for the two pathogens to successfully reproduce in numbers high enough to cause anaerobic respiration and chemical electric reactions.

2.4 Stage 2 - Propagation [24h]

The host will be in intense pain, experiencing migraine, and suffer intermittent psychosis including aggression, hyperphagia and likely hallucination. The host will often scratch at themselves in attempt to alleviate pain, in doing so causing open wounds increasing chance of contagion.

Uncrontrolled movements such as twitching may be evident and sores and bruising will be noticible. Fever will have intensified giving the host a sullen appearance.

At this stage

2.5 Stage 3 - Final [36h]

Massive organ failure due to liquification.

Massive brain dysfunction has occurred.

Clinical death is the foremost result.

Most parts of the brain will have been assimilated by lyssasangre and are being broken down by halinespiro, providing significant quantities of ATP to the remaining brain tissue. This in effect provides the energy required for semi aware movement and the most significant sensation evident in the host before death. In almost all cases this is severe hyperphagia specifically for protein rich sustenance. The host has enough awareness to recognise food in the form of mammalian flesh tissue.

The stomach lining either remains in part or is dissolved, such that any ingested particles will be immediately attacked by the halinespirovirus and harvested for protein, which will be converted to ATP. The brain and muscle tissue will fed this cellular energy across the still active muscle and nerve cells.

The host will be seen to have an ungainly walk due to muscle stiffness, and lack of acute motor skills and balance. This is startling development considering the host being clinically dead. Some hosts are capable, if not barely, to climb small inclines and even impact upper limbs against objects.