Yersinia pestis

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Yersinia pestis
Yersinia pestis.jpg
A scanning electron micrograph depicting a mass of Yersinia pestis bacteria in the foregut of an infected flea
Scientific classification Red Pencil Icon.png
Domain: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Yersiniaceae
Genus: Yersinia
Y. pestis
Binomial name
Yersinia pestis
(Lehmann & Neumann, 1896)
van Loghem, 1944


  • Bacille de la peste
    Yersin, 1894
  • Bacterium pestis
    Lehmann & Neumann, 1896
  • Pasteurella pestis
    (Lehmann & Neumann, 1896) The Netherlands, 1920

Yersinia pestis (formerly Pasteurella pestis) is a gram-negative, non-motile, rod-shaped, coccobacillus bacterium, without spores. It is a facultative anaerobic organism that can infect humans via the Oriental rat flea (Xenopsylla cheopis). [1] It causes the disease plague, which takes three main forms: pneumonic, septicemic, and bubonic. [1] [2]


All three forms have been responsible for high-mortality epidemics throughout human history, including the Plague of Justinian in the sixth century; the Black Death, which accounted for the death of at least one-third of the European population between 1347 and 1353; and the Third Pandemic, sometimes referred to as the Modern Plague, which began in the late 19th century in China and spread by rats on steamships, claiming close to 10 million lives. [3] [4] [5] [6]

Those plagues may have originated in Central Asia or China and were transmitted west via trade routes. [7] [6] [8] However, research in 2018 found evidence of the pathogen in an ancient Swedish tomb, which may have been the cause of what has been described as the Neolithic decline around 3000 BC, in which European populations declined significantly. [9] This would suggest that Y. pestis may have originated in Europe in the Cucuteni–Trypillia culture instead of Asia. [10]

Y. pestis was discovered in 1894 by Alexandre Yersin, a Swiss/French physician and bacteriologist from the Pasteur Institute, during an epidemic of the plague in Hong Kong. [11] Yersin was a member of the Pasteur school of thought. Kitasato Shibasaburō, a Japanese bacteriologist who practised Koch's methodology, was also engaged at the time in finding the causative agent of the plague. [12] However, Yersin actually linked plague with Y. pestis. Formerly named Pasteurella pestis, the organism was renamed Yersinia pestis in 1944.

Every year, thousands of cases of the plague are still reported to the World Health Organization, although with proper antibiotic treatment, the prognosis for victims is now much better. A five- to six-fold increase in cases occurred in Asia during the time of the Vietnam War, possibly due to the disruption of ecosystems and closer proximity between people and animals. The plague is now commonly found in sub-Saharan Africa and Madagascar, areas that now account for over 95% of reported cases. The plague also has a detrimental effect on nonhuman mammals. [13] In the United States, mammals such as the black-tailed prairie dog and the endangered black-footed ferret are under threat.

General characteristics

Y. pestis is a nonmotile, stick-shaped, facultative anaerobic bacterium with bipolar staining (giving it a safety pin appearance) that produces an antiphagocytic slime layer. [14] Similar to other Yersinia species, it tests negative for urease, lactose fermentation, and indole. [15] Its closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis , and more distantly Yersinia enterocolitica .


A complete genomic sequence is available for two of the three subspecies of Y. pestis: strain KIM (of biovar Y. p. medievalis), [16] and strain CO92 (of biovar Y. p. orientalis, obtained from a clinical isolate in the United States). [17] As of 2006, the genomic sequence of a strain of biovar Antiqua has been recently completed. [18] Similar to the other pathogenic strains, signs exist of loss of function mutations. The chromosome of strain KIM is 4,600,755 base pairs long; the chromosome of strain CO92 is 4,653,728 base pairs long. Like Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. It also hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1 (also called pFra) that are not carried by the other Yersinia species. pFra codes for a phospholipase D that is important for the ability of Y. pestis to be transmitted by fleas. [19] pPla codes for a protease, Pla, that activates plasmin in human hosts and is a very important virulence factor for pneumonic plague. [20] Together, these plasmids, and a pathogenicity island called HPI, encode several proteins that cause the pathogenesis, for which Y. pestis is famous. Among other things, these virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria in the host cell (via a type-III secretion system), and acquisition and binding of iron harvested from red blood cells (by siderophores). Y. pestis is thought to be descended from Y. pseudotuberculosis , differing only in the presence of specific virulence plasmids.

A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006. [21] The analysis focused on the transition to a growth condition mimicking growth in host cells.

Small noncoding RNA

Numerous bacterial small noncoding RNAs have been identified to play regulatory functions. Some can regulate the virulence genes. Some 63 novel putative sRNAs were identified through deep sequencing of the Y. pestis sRNA-ome. Among them was Yersinia-specific (also present in Y. pseudotuberculosis and Y. enterocolitica) Ysr141 (Yersinia small RNA 141). Ysr141 sRNA was shown to regulate the synthesis of the type III secretion system (T3SS) effector protein YopJ. [22] The Yop-Ysc T3SS is a critical component of virulence for Yersinia species. [23] Many novel sRNAs were identified from Y. pestis grown in vitro and in the infected lungs of mice suggesting they play role in bacterial physiology or pathogenesis. Among them sR035 predicted to pair with SD region and transcription initiation site of a thermo-sensitive regulator ymoA, and sR084 predicted to pair with fur, ferric uptake regulator. [24]

Pathogenesis and immunity

Oriental rat flea (Xenopsylla cheopis) infected with the Y. pestis bacterium, which appears as a dark mass in the gut: The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis is regurgitated into the wound, causing infection. Flea infected with yersinia pestis.jpg
Oriental rat flea (Xenopsylla cheopis) infected with the Y. pestis bacterium, which appears as a dark mass in the gut: The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis is regurgitated into the wound, causing infection.

In the urban and sylvatic (forest) cycles of Y. pestis, most of the spreading occurs between rodents and fleas. In the sylvatic cycle, the rodent is wild, but in the urban cycle, the rodent is primarily the brown rat (Rattus norvegicus). In addition, Y. pestis can spread from the urban environment and back. Transmission to humans is usually through the bite of infected fleas. If the disease has progressed to the pneumonic form, humans can spread the bacterium to others by coughing, vomiting, and possibly sneezing.

In reservoir hosts

Several species of rodents serve as the main reservoir for Y. pestis in the environment. In the steppes, the natural reservoir is believed to be principally the marmot. In the western United States, several species of rodents are thought to maintain Y. pestis. However, the expected disease dynamics have not been found in any rodent. Several species of rodents are known to have a variable resistance, which could lead to an asymptomatic carrier status. [25] Evidence indicates fleas from other mammals have a role in human plague outbreaks. [26]

The lack of knowledge of the dynamics of plague in mammal species is also true among susceptible rodents such as the black-tailed prairie dog (Cynomys ludovicianus), in which plague can cause colony collapse, resulting in a massive effect on prairie food webs. [27] However, the transmission dynamics within prairie dogs do not follow the dynamics of blocked fleas; carcasses, unblocked fleas, or another vector could possibly be important, instead. [28]

In other regions of the world, the reservoir of the infection is not clearly identified, which complicates prevention and early-warning programs. One such example was seen in a 2003 outbreak in Algeria. [29]


The transmission of Y. pestis by fleas is well characterized. [30] Initial acquisition of Y. pestis by the vector occurs during feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage system and Yersinia murine toxin (Ymt). Although Ymt is highly toxic to rodents and was once thought to be produced to ensure reinfection of new hosts, it is important for the survival of Y. pestis in fleas. [19]

The hemin storage system plays an important role in the transmission of Y. pestis back to a mammalian host. [31] While in the insect vector, proteins encoded by hemin storage system genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus. [32] [33] The presence of this biofilm seems likely to be required for stable infection of the flea. [34] Aggregation in the biofilm inhibits feeding, as a mass of clotted blood and bacteria forms (referred to as "Bacot's block" after entomologist A.W. Bacot, the first to describe this phenomenon). [35] Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria lodged in the proventriculus, which is regurgitated back into the host circulatory system. [35]

In humans and other susceptible hosts

Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors, including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses a plasmin activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots to facilitate systematic invasion. [20] Many of the bacteria's virulence factors are antiphagocytic in nature. Two important antiphagocytic antigens, named F1 (fraction 1) and V or LcrV, are both important for virulence. [14] These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils. [36]

In addition, the type-III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins, called Yersinia outer proteins (Yops), include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The YopO, YopH, YopM, YopT, YopJ, and YopE are injected into the cytoplasm of host cells by T3SS into the pore created in part by YopB and YopD. [37] The injected Yops limit phagocytosis and cell signaling pathways important in the innate immune system, as discussed below. In addition, some Y. pestis strains are capable of interfering with immune signaling (e.g., by preventing the release of some cytokines).

Y. pestis proliferates inside lymph nodes, where it is able to avoid destruction by cells of the immune system such as macrophages. The ability of Y. pestis to inhibit phagocytosis allows it to grow in lymph nodes and cause lymphadenopathy. YopH is a protein tyrosine phosphatase that contributes to the ability of Y. pestis to evade immune system cells. [38] In macrophages, YopH has been shown to dephosphorylate p130Cas, Fyb (Fyn binding protein) SKAP-HOM and Pyk, a tyrosine kinase homologous to FAK. YopH also binds the p85 subunit of phosphoinositide 3-kinase, the Gab1, the Gab2 adapter proteins, and the Vav guanine nucleotide exchange factor.

YopE functions as a GTPase-activating protein for members of the Rho family of GTPases such as RAC1. YopT is a cysteine protease that inhibits RhoA by removing the isoprenyl group, which is important for localizing the protein to the cell membrane. YopE and YopT has been proposed to function to limit YopB/D-induced cytolysis. [39] This might limit the function of YopB/D to create the pores used for Yop insertion into host cells and prevent YopB/D-induced rupture of host cells and release of cell contents that would attract and stimulate immune system responses.

YopJ is an acetyltransferase that binds to a conserved α-helix of MAPK kinases. [40] YopJ acetylates MAPK kinases at serines and threonines that are normally phosphorylated during activation of the MAP kinase cascade. [41] [42] YopJ is activated in eukaryotic cells by interaction with target cell phytic acid (IP6). [43] This disruption of host cell protein kinase activity causes apoptosis of macrophages, and this is proposed to be important for the establishment of infection and for evasion of the host immune response. YopO is a protein kinase also known as Yersinia protein kinase A (YpkA). YopO is a potent inducer of human macrophage apoptosis. [44]

It has also been suggested that a bacteriophage  – Ypφ – may have been responsible for increasing the virulence of this organism. [45]

Depending on which form of the plague with which the individual becomes infected, the plague develops a different illness; however, the plague overall affects the host cell’s ability to communicate with the immune system, hindering the body to bring phagocytic cells to the area of infection.

Y. pestis is a versatile killer. In addition to rodents and humans, it is known to have killed camels, chickens, and pigs. [46] Domestic dogs and cats are susceptible to plague, as well, but cats are more likely to develop illness when infected. In either, the symptoms are similar to those experienced by humans, and can be deadly to the animal. People can be exposed by coming into contact with an infected animal (dead or alive), or inhaling infectious droplets that a sick dog or cat has coughed into the air. [47] [48]


A formalin-inactivated vaccine was in the past[ when? ] available in the United States for adults at high risk of contracting the plague until removal from the market by the Food and Drug Administration. It was of limited effectiveness and could cause severe inflammation. Experiments with genetic engineering of a vaccine based on F1 and V antigens are underway and show promise. However, bacteria lacking antigen F1 are still virulent, and the V antigens are sufficiently variable such that vaccines composed of these antigens may not be fully protective. [49] The United States Army Medical Research Institute of Infectious Diseases has found that an experimental F1/V antigen-based vaccine protects crab-eating macaques, but fails to protect African green monkey species. [50] A systematic review by the Cochrane Collaboration found no studies of sufficient quality to make any statement on the efficacy of the vaccine. [51]

Isolation and identification

Y. pestis isolated by Ricardo Jorge [pt] during the 1899 Porto plague outbreak Preparacoes de Ricardo Jorge do bacilo da peste bubonica no Porto (1899) - fotografias de Antonio Placido da Costa (Museu de Historia da Medicina Maximiano Lemos, FMUP).png
Y. pestis isolated by Ricardo Jorge  [ pt ] during the 1899 Porto plague outbreak

In 1894, two bacteriologists, Alexandre Yersin of Switzerland and Kitasato Shibasaburō of Japan, independently isolated in Hong Kong the bacterium responsible for the Third Pandemic. Though both investigators reported their findings, a series of confusing and contradictory statements by Kitasato eventually led to the acceptance of Yersin as the primary discoverer of the organism. Yersin named it Pasteurella pestis in honor of the Pasteur Institute, where he worked. In 1967, it was moved to a new genus and renamed Yersinia pestis in his honor. Yersin also noted that rats were affected by plague not only during plague epidemics, but also often preceding such epidemics in humans and that plague was regarded by many locals as a disease of rats; villagers in China and India asserted that when large numbers of rats were found dead, plague outbreaks soon followed.[ citation needed ]

In 1898, French scientist Paul-Louis Simond (who had also come to China to battle the Third Pandemic) discovered the rat–flea vector that drives the disease. He had noted that persons who became ill did not have to be in close contact with each other to acquire the disease. In Yunnan, China, inhabitants would flee from their homes as soon as they saw dead rats, and on the island of Formosa (Taiwan), residents considered the handling of dead rats heightened the risks of developing plague. These observations led him to suspect that the flea might be an intermediary factor in the transmission of plague, since people acquired plague only if they were in contact with rats that had died less than 24 hours before. In a now classic experiment, Simond demonstrated how a healthy rat died of the plague after infected fleas had jumped to it from a rat that had recently died of the plague. [52] The outbreak spread to Chinatown, San Francisco, from 1900 to 1904 and then to Oakland and the East Bay from 1907 to 1909. [53] It has been present in the rodents of western North America ever since, as fear of the consequences of the outbreak on trade caused authorities to hide the dead of the Chinatown residents long enough for the disease to be passed to widespread species of native rodents in outlying areas. [54]

Ancient DNA evidence

In 2018, the emergence and spread of the pathogen during the Neolithic decline (as far back as 6,000 years ago) was published. [10] A site in Sweden was the source of the DNA evidence and trade networks were proposed as the likely avenue of spread rather than migrations of populations.

DNA evidence published in 2015 indicates Y. pestis infected humans 5,000 years ago in Bronze Age Eurasia, [55] but genetic changes that made it highly virulent did not occur until about 4,000 years ago. [56] The highly virulent version capable of transmission by fleas through rodents, humans, and other mammals was found in two individuals associated with the Srubnaya culture from the Samara region in Russia from around 3,800 years ago and an Iron Age individual from Kapan, Armenia from around 2,900 years ago. [56] [55] This indicates that at least two lineages of Y. pestis were circulating during the Bronze Age in Eurasia. [56] The Y. pestis bacterium has a relatively large number of nonfunctioning genes and three "ungainly" plasmids, suggesting an origin less than 20,000 years ago. [46]

Three main strains are recognised: Y. p. antiqua, which caused a plague pandemic in the sixth century; Y. p. medievalis, which caused the Black Death and subsequent epidemics during the second pandemic wave; and Y. p. orientalis, which is responsible for current plague outbreaks. [57]

Recent events

In 2008, the plague was commonly found in sub-Saharan Africa and Madagascar, areas that accounted for over 95% of the reported cases. [13]

In September 2009, the death of Malcolm Casadaban, a molecular genetics professor at the University of Chicago, was linked to his work on a weakened laboratory strain of Y. pestis. [58] Hemochromatosis was hypothesised to be a predisposing factor in Casadaban's death from this attenuated strain used for research. [59]

In 2010, researchers in Germany definitely established, using PCR evidence from samples obtained from Black Death victims, that Y. pestis was the cause of the medieval Black Death. [60]

In 2011, the first genome of Y. pestis isolated from Black Death victims was published, and concluded that this medieval strain was ancestral to most modern forms of Y. pestis. [61]

In 2015, Cell published results from a study of ancient graves. [62] Plasmids of Y. pestis were detected in archaeological samples of the teeth of seven Bronze Age individuals, in the Afanasievo culture in Siberia, the Corded Ware culture in Estonia, the Sintashta culture in Russia, the Unetice culture in Poland, and the Andronovo culture in Siberia. [63]

On September 8, 2016, the Y. pestis bacterium was identified from DNA in teeth found at a Crossrail building site in London. The human remains were found to be victims of the Great Plague of London, which lasted from 1665 to 1666. [64]

On January 15, 2018, researchers at the University of Oslo and the University of Ferrara suggested that humans and their parasites were the biggest carriers of the plague. [65] [66]

On November 3, 2019, two cases of pneumonic plague were diagnosed at a hospital in Beijing's Chaoyang district, prompting fears of an outbreak. Doctors diagnosed a middle-aged man with fever, who had complained of difficulty breathing for some ten days, accompanied by his wife with similar symptoms. [67] Police quarantined the emergency room at the hospital and controls were placed on Chinese news aggregators. [67] On the 18th, a third case was reported in a 55-year-old male from Xilingol League, one of the twelve Mongolic autonomous regions in Northern China. The patient received treatment and 28 symptomless contacts were placed in quarantine. [68]

In July 2020, officials increased precautions after a case of bubonic plague was confirmed in Bayannur, a city in China's Inner Mongolia autonomous region. The patient was quarantined and treated. According to China's Global Times, a second suspected case was also investigated, and a level 3 alert was issued, in effect until the end of the year. It forbade hunting and eating of animals that could carry plague and called on the public to report suspected cases. [69]

Related Research Articles

Black Death Mid-14th century pandemic in Eurasia and North Africa

The Black Death was the deadliest pandemic recorded in human history. The Black Death resulted in the deaths of up to 75–200 million people in Eurasia and North Africa, peaking in Europe from 1347 to 1351. Plague, the disease caused by the bacterium Yersinia pestis, was the cause; Y. pestis infection most commonly results in bubonic plague, but can cause septicaemic or pneumonic plagues.

Plague (disease) Specific contagious and frequently fatal human disease caused by Yersinia pestis

Plague is an infectious disease caused by the bacterium Yersinia pestis. Symptoms include fever, weakness and headache. Usually this begins one to seven days after exposure. In the bubonic form there is also swelling of lymph nodes, while in the septicemic form tissues may turn black and die, and in the pneumonic form shortness of breath, cough and chest pain may occur.

<i>Yersinia</i> genus of bacteria

Yersinia is a genus of bacteria in the family Yersiniaceae. Yersinia species are Gram-negative, coccobacilli bacteria, a few micrometers long and fractions of a micrometer in diameter, and are facultative anaerobes. Some members of Yersinia are pathogenic in humans; in particular, Y. pestis is the causative agent of the plague. Rodents are the natural reservoirs of Yersinia; less frequently, other mammals serve as the host. Infection may occur either through blood or in an alimentary fashion, occasionally via consumption of food products contaminated with infected urine or feces.

Braun's lipoprotein, found in some gram-negative cell walls, is one of the most abundant membrane proteins; its molecular weight is about 7.2 kDa. It is bound at its C-terminal end by a covalent bond to the peptidoglycan layer and is embedded in the outer membrane by its hydrophobic head. BLP tightly links the two layers and provides structural integrity to the outer membrane.

<i>Francisella tularensis</i> species of bacterium

Francisella tularensis is a pathogenic species of Gram-negative coccobacillus, an aerobic bacterium. It is nonspore-forming, nonmotile, and the causative agent of tularemia, the pneumonic form of which is often lethal without treatment. It is a fastidious, facultative intracellular bacterium, which requires cysteine for growth. Due to its low infectious dose, ease of spread by aerosol, and high virulence, F. tularensis is classified as a Tier 1 Select Agent by the U.S. government, along with other potential agents of bioterrorism such as Yersinia pestis, Bacillus anthracis, and Ebola virus. When found in nature, Francisella tularensis can survive for several weeks at low temperatures in animal carcasses, soil, and water. In the laboratory, F. tularensis appears as small rods, and is grown best at 35–37 °C.

<i>Yersinia enterocolitica</i> species of bacterium

Yersinia enterocolitica is a Gram-negative, bacillus-shaped bacterium, belonging to the family Yersiniaceae. It is motile at temperatures of 22–29° C (72-84°F), but becomes nonmotile at normal human body temperature. Y. enterocolitica infection causes the disease yersiniosis, which is an animal-borne disease occurring in humans, as well as in a wide array of animals such as cattle, deer, pigs, and birds. Many of these animals recover from the disease and become carriers; these are potential sources of contagion despite showing no signs of disease. The bacterium infects the host by sticking to its cells using trimeric autotransporter adhesins.

<i>Yersinia pseudotuberculosis</i> species of bacterium

Yersinia pseudotuberculosis is a Gram-negative bacterium that causes Far East scarlet-like fever in humans, who occasionally get infected zoonotically, most often through the food-borne route. Animals are also infected by Y. pseudotuberculosis. The bacterium is urease positive.

Virulence factors are molecules produced by bacteria, viruses, fungi, and protozoa that add to their effectiveness and enable them to achieve the following:

Bubonic plague Human and animal disease

Bubonic plague is one of three types of plague caused by bacterium Yersinia pestis. One to seven days after exposure to the bacteria, flu-like symptoms develop. These symptoms include fever, headaches, and vomiting. Swollen and painful lymph nodes occur in the area closest to where the bacteria entered the skin. Occasionally, the swollen lymph nodes may break open.


In molecular biology, LcrV is a protein found in Yersinia pestis and several other bacterial species. It forms part of the Yersinia pestis virulence protein factors that also includes all Yops, or Yersinia outer protein, but the name has been kept out of convention. LcrV's main function is not actually known, but it is essential for the production of other Yops.

Theories of the Black Death are a variety of explanations that have been advanced to explain the nature and transmission of the Black Death (1347–51). A number of epidemiologists and since the 1980s have challenged the traditional view that the Black Death was caused by plague based on the type and spread of the disease. The confirmation in 2010 and 2011 that Yersinia pestis DNA was associated with a large number of plague sites has renewed focus on plague as the leading hypothesis, but has not yet led to a final resolution of all these questions.

Plague vaccine vaccine used against Yersinia pestis

Plague vaccine is a vaccine used against Yersinia pestis. Dead bacteria have been used since 1890 but are less effective against pneumonic plague so that recently live vaccines of an attenuated type and recombination protein vaccines have been developed to prevent the disease.

Yersiniabactin chemical compound

Yersiniabactin (Ybt) is a siderophore found in the pathogenic bacteria Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica, as well as several strains of enterobacteria including enteropathogenic Escherichia coli and Salmonella enterica. Siderophores, compounds of low molecular mass with high affinities for ferric iron, are important virulence factors in pathogenic bacteria. Iron—an essential element for life used for such cellular processes as respiration and DNA replication—is extensively chelated by host proteins like lactoferrin and ferritin; thus, the pathogen produces molecules with an even higher affinity for Fe3+ than these proteins in order to acquire sufficient iron for growth. As a part of such an iron-uptake system, yersiniabactin plays an important role in pathogenicity of Y. pestis, Y. pseudotuberculosis, and Y. entercolitica.

YopH, N-terminal

In molecular biology, YopH, N-terminal refers to an evolutionary conserved protein domain. This entry represents the N-terminal domain of YopH protein tyrosine phosphatase (PTP).

YopE protein domain InterPro Domain

In molecular biology, the protein domain YopE refers to the secretion of virulence factors in Gram-negative bacteria involves transportation of the protein across two membranes to reach the cell exterior. It not only infects the host cell but also protects the bacteria. It undergoes several mechanisms to evade the host's immune system. This particular protein domain can be referred to as a Rho GTPase-activating protein (GAP).

YopR bacterial protein domain

In molecular biology, YopR is a protein domain commonly found in gram negative bacteria, in particular Yersinia and is a core domain. Proteins in this entry are type III secretion system effectors. They are named differently in different species and in Yersinia has been designated YopR which is encoded by the YscH gene. This Yop protein is unusual in that it is released to the extracellular environment rather than injected directly into the target cell as are most Yop proteins. A hallmark of Yersinia type III machines is the presence of needles extending from the bacterial surface. Needles perform two functions, firstly, as a channel to export effectors into the immune cells and secondly as a sensor.

YadA bacterial adhesin protein domain type of protein

In molecular biology, YadA is a protein domain which is short for Yersinia adhesin A. These proteins have strong sequence and structural homology, particularly at their C-terminal end. The function is to promote their pathogenicity and virulence in host cells, though cell adhesion. YadA is found in three pathogenic species of Yersinia, Y. pestis,Y. pseudotuberculosis, and Y. enterocolitica. The YadA domain is encoded for by a virulence plasmid in Yersinia, which encodes a type-III secretion (T3S) system consisting of the Ysc injectisome and the Yop effectors.

Yersinia virus L413C is a virus of the family Myoviridae, genus Peduovirus.

Bacterial effectors are proteins secreted by pathogenic bacteria into the cells of their host, usually using a type 3 secretion system (TTSS/T3SS), a type 4 secretion system (TFSS/T4SS) or a Type VI secretion system (T6SS). Some bacteria inject only a few effectors into their host’s cells while others may inject dozens or even hundreds. Effector proteins may have many different activities, but usually help the pathogen to invade host tissue, suppress its immune system, or otherwise help the pathogen to survive. Effector proteins are usually critical for virulence. For instance, in the causative agent of plague, the loss of the T3SS is sufficient to render the bacteria completely avirulent, even when they are directly introduced into the bloodstream. Gram negative microbes are also suspected to deploy bacterial outer membrane vesicles to translocate effector proteins and virulence factors via a membrane vesicle trafficking secretory pathway, in order to modify their environment or attack/invade target cells, for example, at the host-pathogen interface.

Ancientpathogengenomics is a scientific field related to the study of pathogen genomes recovered from ancient human, plant or animal remains. Ancient pathogens are microorganisms, now extinct, that in the past centuries caused several epidemics and deaths worldwide. Their genome, to which we referred as ancient DNA (aDNA), is isolated from the burial's remains of victims of the pandemics caused by these pathogens.


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