Cycle duration depends on the Plasmodium strain (24, 48, or 72 hours).
Some individuals experience only one cycle before dormancy.
Dormancy can last weeks, months, or even years.
Severe cases: anemia develops (caused by Plasmodium invading and rupturing red blood cells).
Throughout cold and hot phases: vomiting, diarrhea (possibly bloody), muscle/joint pain, convulsions, seizures, delirium.
Death usually occurs in a hospital due to high fever causing brain damage.
Life Cycle of Plasmodium
Two parts: inside the insect and inside the animal host.
Other mammals (primates) and birds can also get malaria.
Female mosquito takes a blood meal containing gametocytes if the host is infected.
Gametocytes (young, immature Plasmodium) undergo sexual reproduction in the mosquito's midgut if two mating types (+/-) are present.
Oocyst is produced.
The mosquito digestive system has 3 chambers that includes the foregut, midgut and hindgut.
In the foregut, the red blood cells will be degraded and contents of red blood cells are released.
If two mating types are present, sexual reproduction occurs in the midgut to produce an oocyst. Oocyst then moves into the hindgut.
Oocyst ruptures to release sporozoites.
Sporozoites migrate to the salivary gland.
Next blood meal injects Plasmodium into the host.
In the host (e.g., human), sporozoites are injected into bloodstream, travel to the liver, and mature into schizonts.
Schizonts rupture, releasing merozoites.
Merozoites invade red blood cells.
Red blood cell is altered to prevent further merozoite entry.
Merozoites develop into trophozoites (early, late stages) and then schizonts, filling the red blood cell.
Red blood cell ruptures, releasing merozoites, repeating the cycle.
Cycle length (24, 48, 72 hours) is how long this process takes in the host.
Symptoms correlate with the life cycle stages:
Merozoites leaving the liver trigger low-grade fever (cold phase).
Asexual reproduction inside red blood cells leads to cells filled with schizonts and trophozoites which ruptures at the same time causing the hot phase.
Immune system raises temperature during the burst effect.
Merozoites race to enter other red blood cells.
Immune system senses absence of free merozoites, fever breaks (wet phase).
Symptoms reoccur with each new burst.
Microscopic Observations
Pink cells: red blood cells.
Purple bodies inside pink cells: red blood cells infected with Plasmodium (various stages).
Anopheles mosquito injects sporozoites into the host via saliva.
Sporozoites travel to liver cells and mature into schizonts.
Schizonts rupture, release merozoites into the bloodstream.
One merozoite enters each red blood cell, modifying it.
Red blood cell fills with Plasmodium; ruptures, releasing merozoites.
Occasionally, early trophozoites develop into gametocytes (taken up during the next mosquito blood meal).
Responsible for most diseases, especially in developed countries.
Not considered alive because they don't meet all criteria for living things.
Cannot metabolize, grow, replicate independently, or respond to the environment.
Recruit host cell's metabolic pathways for replication.
No cytoplasmic membrane, cytoplasm, cytosol, or organelles usually.
Extracellular (virion) and intracellular state.
Virion
Composed of a protein coat (capsid) covering nucleic acid.
Nucleic acid + capsid = nucleocapsid.
Some have a phospholipid envelope (host cell membrane).
Outermost layer provides protection and recognition sites for host cells.
Capsid: made of protein subunits (capsomeres).
Capsid Removal
Inside the host cell, the capsid is removed, and DNA or RNA is released.
Nucleic acid causes disease.
Viruses take over host cell ribosomes to make viral protein.
Either DNA or RNA (not both).
Classified as either DNA or RNA viruses.
Can be double-stranded or single-stranded.
Linear, circular, or segmented.
Relatively small genome with not many genes.
Host Specificity
Viruses must attach to an appropriate host cell.
Attachment fibers (spikes) on virus fit perfectly into receptor sites on host cells.
Receptor sites must allow attachment.
If no appropriate cell/attachment, no infection.
Viral Shapes
Capsomere arrangement determines shape.
Icosahedral: arrange to form triangular faces.
Helical: capsomere arrange in a tube to form a capsid.
Bacteriophages: shown here.
Enveloped viruses: Surrounded by host cell membrane. Naked viruses are not enveloped viruses are more at risk of being dried out as its outside of a host.
Viral Replication: Lytic Cycle
Lytic Cycle of Replication includes the Attachment, inject/Insert/Entry/ Insertion, Integration +-, Synthesis. Assembly Release.
In this cycle the genetic material from the virus is incorporated into the host.
Attachment: virus attaches to a host cell and has it's receptor fit perfectly to host cell.
Injection/Entry : Is brought into the host cell.
Insertion +-: The genetic material of the virus is escorted to the nucleus where its incorporated in the host genome. Every-time host cell replications it will be copying the DNA.
Synthesis: Production of components of virus in the host cells.
Assembly: Assembles all components of the virus.
Release: Virus is being released in 2 ways a Naked virus meaning that it breaks out of the host or release from a host cell, viruses buds out one at a time.
B cells produce antibodies, covering parts of the virus called attachment fibers and prevents them from attaching to a host cell.
Naked virus gets detected much earlier and enveloped viruses are very likely to protect from immunity.
Viral Replication: Lysogenic Cycle
LYSOGENIC involves being the opposite. Starts and is still a cycle of reproduction.
Insertion, integration. Then there is the period of dormancy. This period doesn't show symptoms.
Evolutionary reasons why a virus has dormancy is that it can remain dormant until weakening of the host occurs. There are chemical changes that cause it . Sunlight to get it out of dormancy.
Following from that it's the same step.
Infection- If no appropriate cell/attachment, no infection.
Transformative Viruses
Not only do they take over a whole cell and make them do something new, but they can also, in some cases, be a neoplastic virus or a neo can result in neoplasia.
Cause cancer by transforming host cells and is benign and is in some long term and cause harm
Transformation results in the old host cells job is nothing and it just replicates as viruses
HPV, all tend to be HPV.
Methods of studying Virus
Tissue test.
Can't be grown in dishes has to be grown in tissue and the injection virus is injected in chicken and cultivated.
Immune Function
Viruses need to break the immune system to cause diseases this can be broken down into 2 part specific and non specific.
Non specific immunity which is the innate immunity that doesnt target any pathogen however this doesn't have memory.
More important probably specific immunity or adaptive immunity is respond to particular antigen or anything foreign. This will generate memory.
Non specific includes all the Flora or Microbes, lymph system chemical barrier, reflexes hormones inflammation. However it doesnt generates memory.. How Interferon works.
Interferon
Interfoon is a nonanti body protein that activate antiviral protectants and viruses and isnt species specific . However its labile. Not produce in the first trimester of pregnancy. This makes the infant suseptical..
Specific Immunity
Put into 2 types of cells. Tcells and B CELLS.
Bcells produce antibodies and detect all things foreign.
B cells cant operate without order and relies on other Tcells that can direct them where to go and what to do.