Als Relegation zur deutschen Fußball-Bundesliga werden im deutschen Ligafußball die . Der 1. FC Nürnberg nahm bereits zum dritten Mal teil. Der Hamburger SV sowie der VfL Wolfsburg nahmen bisher zweimal teil. Mai Wolfsburg hat sich durch ein gegen Köln den Relegationsplatz gesichert. Der HSV steigt damit zum ersten Mal ab. Das Spiel der. Mai Der Spieltag der Bundesliga ist vorbei, alle Entscheidungen sind durch. Der HSV steigt ab, der VfL Wolfsburg muss in die Relegation.
Eventually in the next season Hamburg once again changed managers due to a poor start of the season firing Slomka on 15 September. His successor Josef Zinnbauer held the job up until 22 March and was replaced by interim coach Peter Knäbel.
Labbadia achieved only two points in the first ten games of the —17 season and was replaced by Markus Gisdol who had a shaky start but managed to get 20 points in 9 games from the 19th match day to the 28th match day.
On the last match day, Hamburg avoided the relegation play-offs and stayed in the Bundesliga. However, eight games followed without a single win.
At the end of the first half of the season, HSV was in second last place in the table. After two defeats in the first two games of the second half, coach Markus Gisdol was dismissed.
HSV hired Bernd Hollerbach , a former player of the club, as a new coach. After seven games without a win and a defeat against FC Bayern Munich , he was also dismissed.
On the day of his appointment, he dismissed the sports director Jens Todt. The club hired former successful HSV player Thomas von Heesen as a sports consultant until the end of season.
He should take over a part of the duties for the dismissed Jens Todt. Until then, he was very successful in the Regionalliga Nord fourth league and was with his team at the top of the table.
With four wins and an offensively minded style of play, the coach convinced the club and received a two-year contract. After the disastrous season in the —18 Bundesliga season under three different coaches, a final day win over Borussia Mönchengladbach was not enough to escape after Wolfsburg won against Köln.
Bundesliga for the first time in their 55 year history. Hamburger SV plays its home games in the Volksparkstadion , which was previously known as the Imtech Arena between and HSV fans can be buried at a dedicated graveyard near the home stadium, covered in turf from the original Hamburg pitch.
Pauli came back again, there were already several weeks before the game disputes of both fan groups. It started when about HSV fans interrupt a St.
Pauli concert because it took place on the "HSV-side" of the Reeperbahn. In a league game a short time later, the HSV fans showed a banner in the stadium with the inscription "Stellt euch endlich unsrer Gier - Ihr: After fans of FC St.
Pauli attacked HSV fans working on a choreography for the game and destroyed parts of it, some HSV fans threatened them by hanging figures in the colours of the rival at several bridges throughout the city.
In addition, one day later there was a march of about 80 HSV-Ultras across the Reeperbahn , where insulting chants agains St. Besides, after two major conflicts between the two fan groups the relationship with Holstein Kiel has been considered as difficult for a short time now.
HSV have an affinity with Scottish club Rangers. HSV fans unfurl their club logo at Rangers' away European matches. The link between Rangers and Hamburg dates back to when the Hamburg Rangers Supporters' Club was set up by HSV fans who had visited Rangers matches before and were thrilled by the atmosphere at Ibrox.
The links were further strengthened when Rangers signed Jörg Albertz from Hamburg. In the derby against St. Pauli in the season about fans of the scottish club traveled to Hamburg to support HSV.
Pauli has no influence on this friendship, however. They showed a Union Jack , bearing the words "No Surrender", as a big choreography in the stadium.
The background to this is that Celtic is generally regarded as a club for people who want an independent Scotland, while Glasgow Rangers is regarded as very loyal to Great Britain.
Their meetings involve the visitors' club song to be played, and fans chanting HSV from each end of the stadium. Especially in the s, multiple players transferred between the two clubs.
As Hannover and Bielefeld fans have affinities as well, all three clubs are sometimes called the Nordallianz Northern Alliance despite the fact that the city of Bielefeld is not technically located in Northern Germany.
In addition, some fan groups maintain good contacts with the fourth division team VfB Lübeck , whose fans also have an aversion to St.
Pauli and Holstein Kiel. In , HSV helped the club, which was threatened by insolvency, with a free friendly match, in which the team competed with several national players to attract as many spectators as possible and left the entire earnings for VfB Lübeck.
For some years, there is also a close friendship between ultra-groups of HSV and F. The club colours are officially blue, white and black according to its statute but the fans use the combination "schwarz-weiss-blau" black-white-blue in their songs and chants; they also chant "haa-ess-fow" HSV.
The club crest is a black and white diamond on a blue background. These were the colours of SC Germania. The use of the blue background suggests a link with Hamburg's maritime tradition as the Blue Peter flag signal meaning "All Aboard" or "Outward Bound" is a white rectangle on a similar blue background.
In contrast, the team's home kit is white jerseys and red shorts, which are the colours of the Free and Hanseatic City of Hamburg. As a result, the team's most common nickname is "die Rothosen" the Red Shorts.
Because of its age and having been ever-present in the top flight of German football, HSV is also known as der Dinosaurier the Dinosaur and currently uses a dinosaur mascot called "Hermann" named after long-time club physiotherapist Hermann Rieger for marketing purposes.
HSV's kit was made by Adidas from to   and the club re-engaged Adidas in having worked with a number of its competitors in the meantime.
The first shirt sponsorship was introduced in The shirt now carries the Fly Emirates logo. The following is a list of shirt sponsors by date:.
HSV's first participation in European competition came after they won the German championship in and were invited to take part in the —61 European Cup.
They had a bye in the preliminary round and their first round opponents were Young Boys. HSV won the two-legged tie 8—3 on aggregate, beating the Swiss side 0—5 in the away leg on 2 November and then drawing 3—3 at home on 27 November.
HSV reached the semi-final of the European Cup in Subsequently, they have twice played in the final, losing 1—0 to Nottingham Forest in and defeating Juventus 1—0 in Their biggest defeat was in the second leg of the Super Cup when they lost 6—0 to Liverpool at Anfield on 6 December.
HSV have the record in German football of having won the most regional titles, having won 31 regional titles. The regional titles do however not count as a trophy or even as a title itself.
Winning a regional title only guaranteed a club to battle, with other regional winning clubs, for the German Championship. Hamburg's three Bundesliga championships entitle the club to display one gold star of the "Verdiente Meistervereine".
Under the current award system, their pre-Bundesliga championships are not recognized and so they are not entitled to the second star of a five-time champion.
After the replay of the championship final in had to be abandoned due to the opponents no longer having enough players on the ground, the German Football Association DFB requested HSV to renounce the title, which the club did.
During his first season with Hamburger SV —01 , Sergej Barbarez became the top scorer for his club with 22 goals and joint top scorer of the Bundesliga with Ebbe Sand.
Until the —18 season, HSV took pride in its status as the only club to have played continuously in the Bundesliga since its foundation.
A large clock in the northwest corner of the Volksparkstadion marked the time, down to the second, since the league was founded on 24 August Flags indicate national team as defined under FIFA eligibility rules.
Players may hold more than one non-FIFA nationality. Hamburger SV official website. The reserve team serves mainly as the final stepping stone for promising young players before being promoted to the main team.
The women's section was created in The crucial issue seems to be that the oral mucosa has certain preferred features compared to skin or genital mucosa: The mouth offers more efficient transmission because the virus can be dispersed in aerosols, either released by normal breathing, but more efficiently produced upon coughing or spitting.
Moreover, as enveloped viruses, the herpes family requires moisture for survival. The blisters on the skin serve the purpose as long as they are watery, but the virus relies on skin-to-skin contact with another person, or immediate contact between objects touched by the infected person and the next host.
The occurrence of kissing and food sharing by mouth contribute further to the role of the human mouth in the transmission of pathogens.
Biting is still considered to be a relevant risk factor in the transfer of viruses from other primates Apparently, all herpesviruses have evolved the capacity to access the oral cavity.
VZV, and HSV-1 and -2 are latent in neurons, but the viral particles are transported via axons to mucosa where the virus may continue replicating in epithelial cells.
It should be noted that using the mouth as part of the strategy for viral contagion does not require the formation of sores, blisters, or other visible changes in the mucosa.
However, clinical symptoms associated with the mucosa generally imply a higher abundance of viral particles, and thus a boosted chance of transmission.
Reactivation is a dangerous option for the virus. An active replication will tend to induce various host mechanisms, involving either the immune system or internal signaling in the cell, leading to the death of the infected cell.
For every viral genome that successfully produces infective progeny, several viruses probably initiate this process, but fail at some point along the way.
In order to establish latency, the viral genome is circularized to form an episomal DNA element packed in histones For lytic activation to occur, the genome must be linearized During latency, the viral DNA is copied by cellular DNA polymerases, along with the chromosomes, preferably when the cell engages in mitosis.
This contrasts with lytic replication in which the viral DNA polymerase is engaged, reflecting a viral takeover of the cell.
For latency, the virus relies on the host's epigenetic mechanisms for the silencing of viral genes, such as packaging of the DNA in particular types of histones and specific methylation programs Presumably it is safer to keep the production of viral proteins to a minimum during latency in order to avoid immune surveillance; but at the same time it is important for the virus to be copied in order to maintain long-term presence, as some of the daughter cells will eventually die.
The viral genome is not completely silenced. Latent EBV, for example, expresses a small portion of its genes The virus exhibits three different latency programs, each comprising a limited and distinct set of viral proteins and RNAs 32 , Upon infecting a resting B-cell, the virus starts with the more comprehensive latency III program.
The resulting proteins induce the B-cell to proliferate. The virus subsequently gradually shuts off genes, entering latency II and eventually latency I.
In latency I, only one protein and some non-coding RNAs are expressed. The protein, EBNA-1, binds to a replication origin in the viral genome and is instrumental in securing synthesis of DNA when the host cell divides.
Lytic gene products are also produced in three consecutive stages: The primary role of the immediate-early lytic products is to function as transactivators, enhancing the expression of later lytic genes.
The early lytic products take on more diverse functions, such as replication, metabolism, and blockade of antigen processing.
The late lytic products are typically proteins with structural roles, including the units of the capsid and glycoproteins that are incorporated in the viral envelope.
The actual changes in both viral and host cell transcription and translation over the various stages of viral latency and reactivation are highly complex, as demonstrated with various functional genomics studies on CMV Herpesviruses, being enveloped, normally bud from the cell membrane, which implies that lysis of the cell is not required.
However, the takeover necessary for running active production of viral particles in epithelial cells or leukocytes typically results in cell death.
In the case of HSVs, much of our knowledge of the molecular control of latency comes from studies with virus in cultured neuronal cells Here axonal transport plays an important role.
If the virus first enters at a distant spot on an axon, as compared to closer to the cell body, the situation favors latency.
The explanation may be inefficient axonal transport of virion-associated regulatory factors, such as the HSV lytic initiator protein VP16 The protein is released from the viral particle upon entry, and subsequently requires independent transport to the nucleus in order to initiate the replicative program.
Thus, if the distance to the cell body is large, less VP16 will reach the nucleus, and the onset of viral productivity is compromised.
Later on, other factors may initiate de novo synthesis of VP16 in the nucleus thus causing reactivation. Herpesviruses are known for their ability to establish lifelong infections.
In order to do so they require a strategy for immune evasion, consequently the viruses have evolved a variety of ways to manipulate the immune system of the host.
One typical example is based on molecular mimicry. Most of the viruses encode homologs of cellular interleukins IL , chemokines, or chemokine receptors Another strategy for immune evasion is to reduce the presentation of viral antigens via the major histocompatibility complex MHC of infected cells The manipulation of the immune system offers the reactivated virus at least partial relief from immune surveillance.
It is, however, a feature that increases the risk of the balance tipping toward excessive viral productivity, which is not in the interest of the virus as it can lead to death or serious disability of the host.
Evolution apparently has balanced this possibility, leading to a situation where the viral activity in a normal host is limited to a considerable extent by immune surveillance.
The point is substantiated by the observation that compromised immunity, as in the case of patients receiving immune suppressants, often lead to a drastic increase in viral activity Other data suggest that herpesviruses can in fact form a symbiotic relationship with their hosts.
In a mouse model, it has been shown that the systemic activation of macrophages and the prolonged production of interferon-gamma initiated by herpesviral infections protect against subsequent disease caused by the highly pathogenic bacteria Listeria monocytogenes and Yersinia pestis The suggestion of symbiosis is plausible as it is obviously not in the interest of the virus to have their host succumb to other infections.
In animal models, and most likely in humans as well, reactivation of various herpesviruses can be induced by local trauma e.
An example of the latter is to elevate the body temperature of mice to 43 o C for 10 min The appearance of HSV cold sores correlates with a wide range of stressors, including mental tension, fatigue, and exposure to bright light More than years ago it was shown that applying trauma to a nerve, for example in connection with the treatment of chronic pain, can lead to an outbreak of herpes in the dermatome associated with the nerve Other cell stressors, such as transient interruption of protein synthesis or hypoxia, are sufficient to induce viral activity — an effect that may be mediated by the disruption of mTOR kinase activity This enzyme has a central role in responding to nutritional or to stress-related cellular events by impacting on mRNA translation.
Apparently, in the case of HSV, it is sufficient to inhibit mTOR by chemical means in the distal part of an axon; a signal causing viral reactivation is then sent to the cell body harboring the viral episome.
Presumably, a skin trauma affecting the nerve endings of infected neurons may cause a similar reactivation. In order to maintain latency, the neuron must be functional, active, and healthy.
In cell culture systems, it is also possible to induce reactivation by interfering chemically in ways that impact on gene activity, using compounds that for example block histone methylation or appropriately designed interfering RNAs The question is what factors cause a similar impact on gene expression in vivo.
As to HSV, it is known that environmental triggers such as emotional stress, fever, UV exposure, hormonal changes, dental surgery, and cranial trauma can cause activation 30 ; but it is not known whether these stimuli act directly on the infected neuron, or indirectly by means of bodily functions.
These cells are often found in association with infected neurons, sometimes connected to the neuron via immunological synapses.
They produce interferons and related factors that presumably contribute to the maintenance of latency and at the same time help the neuron survive In the case of EBV, the latent virus harbored in B-cells can be reactivated in vitro by stimulating B-cell receptors, suggesting that reactivation in vivo may occur when the infected B-cell responds to unrelated infections The point may help explain why reactivation of EBV occasionally appears as a secondary infection.
The aging immune system is no longer able to control the virus efficiently leading to a more chronic, slow-and-low rather than latent type of infection A range of deteriorative immunological changes are expected to correlate with aging, but it is not known exactly what causes the concomitant increase in herpesvirus activity.
In fact, the stress associated with space flight is sufficient to cause reactivation of latent herpesviruses, presumably by downregulating cellular immunity 46 ; which suggests that even a minor decline, or change, in immunological function may be enough.
This point is also reflected in the observation that it makes considerable difference whether the individual is first infected as an infant or in puberty, as exemplified by the case of EBV and mononucleosis.
In other words, when CMV and possibly other herpesviruses gradually produces more viral proteins and particles, the concomitant attempt of counteracting the situation by an aging immune system can demote the capacity to fight these viruses.
We have considerable knowledge of the various pathways of molecular signaling that can lead to reactivation, and we have empirical information of environmental triggers doing the same.
What we do not know is which molecular or cellular pathways the environmental factors use. It could be through some of the options outlined by, mostly in vitro , experiments; or it could be novel mechanisms.
Apparently, viral activity depends on a delicate balance of constraining and activating factors. Minor disturbances that upset this balance seem sufficient to lead the virus toward production of progeny, and presumably this disturbance can result from a variety of effectors.
In most cases, reactivation does not lead to serious disease. It is sufficient for the virus to be shed in the oral cavity, and even HSV appears in the saliva in the absence of sores Then again the level of viral activity most likely correlates with clinical symptoms.
Innate and acquired host factors will affect the balance between viral activity and immune surveillance, making some people more susceptible to problematic infections than others.
In this context, it should be mentioned that we tend to attribute guilt by association. If symptoms correlate with the detection of virus, we tend to assume that the virus is responsible.
This may lead to a faulty diagnosis and suboptimal treatment. The herpesviruses are likely to be reactivated as a consequence of a variety of conditions, but they are not necessarily involved in the underlying etiology.
Due to their almost ubiquitous presence and ease of activation, clinical findings and epidemiology may suggest a causative role, even if the viruses are mere opportunists.
The delicate balance between latency and reactivation is designed by evolution. In a normal host, experiencing the normal interaction with the virus, the process is tuned to a long-term relationship that does not cause undue harm.
However, if environmental factors upset this balance, or if the host for whatever reason is immunocompromised, the virus may inadvertently cause disease.
One might speculate that the optimal strategy for counteracting disease is to encourage early life exposure to herpesviruses.
For the average person, infant inoculation with EBV and CMV may be beneficial, but the strategy does imply a risk for disease in rare individuals.
Moreover, we live to an age where it is expected that the immune system has reduced potential, and occasionally we need to subdue the system in connection with various treatments.
Thus, harmful consequences of these viruses are likely to occur at some point in life. One alternative is vaccines.
The more commonly used alternative at the present is medication. Fortunately, we have a considerable pharmaceutical arsenal to fight these viruses 9 , unfortunately these medicines are unlikely to rid the body of virus.
There is no conflict of interest in the present study for any of the author. National Center for Biotechnology Information , U. Journal List J Oral Microbiol v.
Published online Oct Author information Article notes Copyright and License information Disclaimer. Open in a separate window. Footnotes Source of Support: The laboratory diagnosis of herpes simplex virus infections.
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