Editing Infection (section)

===Immunity===
[[File:Mallon-Mary 01.jpg|thumb|[[Mary Mallon]] (a.k.a. Typhoid Mary) was an asymptomatic carrier of [[typhoid fever]]. Over the course of her career as a cook, she infected 53 people, three of whom died.]]
Infection with most pathogens does not result in death of the host and the offending organism is ultimately cleared after the symptoms of the disease have waned.<ref name= Baron/> This process requires [[immune system|immune mechanisms]] to kill or inactivate the [[Inoculation|inoculum]] of the pathogen. Specific acquired [[immunity (medical)|immunity]] against infectious diseases may be mediated by [[Antibody|antibodies]] and/or [[T lymphocyte]]s. Immunity mediated by these two factors may be manifested by:
* a direct effect upon a pathogen, such as antibody-initiated [[complement system|complement]]-dependent bacteriolysis, [[Opsonin|opsonoization]], [[phagocytosis]] and killing, as occurs for some bacteria,
* neutralization of viruses so that these organisms cannot enter cells,
* or by T lymphocytes, which will kill a cell parasitized by a microorganism.

The immune system response to a microorganism often causes symptoms such as a high [[fever]] and [[inflammation]], and has the potential to be more devastating than direct damage caused by a microbe.<ref name=Sherris/>

Resistance to infection ([[immunity (medical)|immunity]]) may be acquired following a disease, by [[asymptomatic carrier|asymptomatic carriage]] of the pathogen, by harboring an organism with a similar structure (crossreacting), or by [[vaccination]]. Knowledge of the protective antigens and specific acquired host immune factors is more complete for primary pathogens than for [[opportunistic pathogen]]s. There is also the phenomenon of [[herd immunity]] which offers a measure of protection to those otherwise vulnerable people when a large enough proportion of the population has acquired immunity from certain infections.<ref name="ofg">{{cite web |title=Herd Immunity |url=http://vk.ovg.ox.ac.uk/herd-immunity |url-status=live |archive-url=https://web.archive.org/web/20190802220355/http://vk.ovg.ox.ac.uk/herd-immunity |archive-date=2 August 2019 |access-date=11 August 2023 |publisher=Oxford Vaccine Group, University of Oxford}}</ref>

Immune resistance to an infectious disease requires a critical level of either antigen-specific antibodies and/or T cells when the host encounters the pathogen. Some individuals develop natural [[blood plasma|serum]] antibodies to the surface [[polysaccharide]]s of some agents although they have had little or no contact with the agent, these natural antibodies confer specific protection to adults and are [[passive immunization|passively transmitted]] to newborns.

====Host genetic factors====
The organism that is the target of an infecting action of a specific infectious agent is called the host. The host harbouring an agent that is in a mature or sexually active stage phase is called the definitive host. The intermediate host comes in contact during the larvae stage. A host can be anything living and can attain to asexual and sexual reproduction.<ref>{{cite journal|vauthors=Barreto ML, Teixeira MG, Carmo EH|year=2006|title=Infectious diseases epidemiology|journal=Journal of Epidemiology and Community Health|volume=60|issue=3|pages=192–95|doi=10.1136/jech.2003.011593|pmc=2465549|pmid=16476746}}</ref>
The clearance of the pathogens, either treatment-induced or spontaneous, it can be influenced by the genetic variants carried by the individual patients. For instance, for genotype 1 [[hepatitis C]] treated with [[Pegylated interferon-alpha-2a]] or [[Pegylated interferon-alpha-2b]] (brand names Pegasys or PEG-Intron) combined with [[ribavirin]], it has been shown that genetic polymorphisms near the human IL28B gene, encoding interferon lambda 3, are associated with significant differences in the treatment-induced clearance of the virus. This finding, originally reported in ''[[Nature (journal)|Nature]]'',<ref>{{cite journal |vauthors=Ge D, Fellay J, Thompson AJ, Simon JS, Shianna KV, Urban TJ, Heinzen EL, Qiu P, Bertelsen AH, Muir AJ, Sulkowski M, McHutchison JG, Goldstein DB | title = Genetic variation in IL28B predicts hepatitis C treatment-induced viral clearance | journal = Nature | volume = 461 | issue = 7262 | pages = 399–401 | year = 2009 | pmid = 19684573 | doi = 10.1038/nature08309 | bibcode = 2009Natur.461..399G | s2cid = 1707096 }}</ref> showed that genotype 1 hepatitis C patients carrying certain genetic variant alleles near the IL28B gene are more possibly to achieve sustained virological response after the treatment than others. Later report from ''Nature''<ref>{{cite journal |vauthors=Thomas DL, Thio CL, Martin MP, Qi Y, Ge D, O'Huigin C, Kidd J, Kidd K, Khakoo SI, Alexander G, Goedert JJ, Kirk GD, Donfield SM, Rosen HR, Tobler LH, Busch MP, McHutchison JG, Goldstein DB, Carrington M | title = Genetic variation in IL28B and spontaneous clearance of hepatitis C virus | journal = Nature | volume = 461 | issue = 7265 | pages = 798–801 | year = 2009 | pmid = 19759533 | pmc = 3172006 | doi = 10.1038/nature08463 | bibcode = 2009Natur.461..798T }}</ref> demonstrated that the same genetic variants are also associated with the natural clearance of the genotype 1 hepatitis C virus.