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  <front>
    <journal-meta>
      <journal-id journal-id-type="eissn">2687-1491</journal-id>
      <journal-title-group>
        <journal-title xml:lang="ru">Журнал медико-биологических исследований</journal-title>
        <journal-title xml:lang="en">Journal of Medical and Biological Research</journal-title>
      </journal-title-group>
      <publisher>
        <publisher-name>Северный (Арктический) федеральный университет</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="doi">10.37482/2687-1491-Z286</article-id>
      <article-id pub-id-type="uri">https://journals.narfu.ru/index.php/med/article/view/2430</article-id>
      <article-categories>
        <subj-group>
          <subject>НАУЧНЫЕ ОБЗОРЫ</subject>
        </subj-group>
        <subj-group>
          <subject>REVIEW ARTICLES</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="ru">Факторы патогенности Anaplasma phagocytophilum (обзор)</article-title>
        <trans-title-group xml:lang="en">
          <trans-title>Pathogenicity Factors of Anaplasma phagocytophilum (Review)</trans-title>
        </trans-title-group>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name name-style="eastern">
            <surname>Гавриш</surname>
            <given-names>Дарья Алексеевна</given-names>
          </name>
          <name-alternatives>
            <name name-style="eastern" xml:lang="ru">
              <surname>Гавриш</surname>
              <given-names>Дарья Алексеевна</given-names>
            </name>
            <name name-style="western" xml:lang="en">
              <surname>Gavrish</surname>
              <given-names>Darya A.</given-names>
            </name>
          </name-alternatives>
          <contrib-id contrib-id-type="orcid">0009-0003-9158-8099</contrib-id>
          <xref ref-type="aff" rid="aff1"/>
        </contrib>
        <contrib contrib-type="author">
          <name name-style="eastern">
            <surname>Саркисян</surname>
            <given-names>Нушик Сааковна</given-names>
          </name>
          <name-alternatives>
            <name name-style="eastern" xml:lang="ru">
              <surname>Саркисян</surname>
              <given-names>Нушик Сааковна</given-names>
            </name>
            <name name-style="western" xml:lang="en">
              <surname>Sarkisyan</surname>
              <given-names>Nushik S.</given-names>
            </name>
          </name-alternatives>
          <contrib-id contrib-id-type="orcid">0000-0003-3512-5738</contrib-id>
          <xref ref-type="aff" rid="aff1"/>
        </contrib>
        <contrib contrib-type="author" corresp="yes">
          <name name-style="eastern">
            <surname>Колодина</surname>
            <given-names>Марина Васильевна</given-names>
          </name>
          <name-alternatives>
            <name name-style="eastern" xml:lang="ru">
              <surname>Колодина</surname>
              <given-names>Марина Васильевна</given-names>
            </name>
            <name name-style="western" xml:lang="en">
              <surname>Kolodina</surname>
              <given-names>Marina V.</given-names>
            </name>
          </name-alternatives>
          <contrib-id contrib-id-type="orcid">0009-0009-2581-2500</contrib-id>
          <xref ref-type="aff" rid="aff1"/>
        </contrib>
        <contrib contrib-type="author">
          <name name-style="eastern">
            <surname>Куличенко</surname>
            <given-names>Александр Николаевич</given-names>
          </name>
          <name-alternatives>
            <name name-style="eastern" xml:lang="ru">
              <surname>Куличенко</surname>
              <given-names>Александр Николаевич</given-names>
            </name>
            <name name-style="western" xml:lang="en">
              <surname>Kulichenko</surname>
              <given-names>Alexandr N.</given-names>
            </name>
          </name-alternatives>
          <contrib-id contrib-id-type="orcid">0000-0002-9362-3949</contrib-id>
          <xref ref-type="aff" rid="aff2"/>
        </contrib>
        <aff-alternatives id="aff1">
          <aff>
            <institution xml:lang="ru">Ставропольский противочумный институт Роспотребнадзора (Ставрополь, Россия)</institution>
          </aff>
          <aff>
            <institution xml:lang="en">Stavropol Plague Control Research Institute (Stavropol, Russia)</institution>
          </aff>
        </aff-alternatives>
        <aff-alternatives id="aff2">
          <aff>
            <institution xml:lang="ru">Ставропольский противочумный институт Роспотребнадзора  (Ставрополь, Россия) (Ставрополь, Россия)</institution>
          </aff>
          <aff>
            <institution xml:lang="en">Stavropol Plague Control Research Institute (Stavropol, Russia)</institution>
          </aff>
        </aff-alternatives>
      </contrib-group>
      <pub-date pub-type="epub" iso-8601-date="2026-05-18">
        <day>18</day>
        <month>05</month>
        <year>2026</year>
      </pub-date>
      <pub-date date-type="collection">
        <year>2026</year>
      </pub-date>
      <volume>14</volume>
      <issue>2</issue>
      <fpage>77</fpage>
      <lpage>90</lpage>
      <history>
        <date date-type="received" iso-8601-date="2025-12-23">
          <day>23</day>
          <month>12</month>
          <year>2025</year>
        </date>
        <date date-type="accepted" iso-8601-date="2026-02-09">
          <day>09</day>
          <month>02</month>
          <year>2026</year>
        </date>
        <date date-type="rev-recd" iso-8601-date="2026-02-05">
          <day>05</day>
          <month>02</month>
          <year>2026</year>
        </date>
      </history>
      <permissions>
        <copyright-statement>© Гавриш Д.А., Саркисян Н.С., Колодина М.В., Куличенко А.Н., 2026</copyright-statement>
        <copyright-year>2026</copyright-year>
        <copyright-holder xml:lang="ru">Гавриш Д.А., Саркисян Н.С., Колодина М.В., Куличенко А.Н.</copyright-holder>
        <copyright-holder xml:lang="en">Gavrish D.A., Sarkisyan N.S., Kolodina M.V., Kulichenko A.N.</copyright-holder>
        <license xlink:href="https://creativecommons.org/licenses/by/4.0/">
          <license-p>CC BY 4.0</license-p>
        </license>
      </permissions>
      <self-uri xlink:type="simple" xlink:href="https://journals.narfu.ru/index.php/med/article/view/2430">https://journals.narfu.ru/index.php/med/article/view/2430</self-uri>
      <abstract xml:lang="ru">
        <p>Гранулоцитарный анаплазмоз человека – природно-очаговая трансмиссивная инфекция, вызываемая облигатным внутриклеточным патогеном Anaplasma phagocytophilum. Актуальность настоящей работы обусловлена ростом интереса к патогенезу анаплазмоза и факторам вирулентности его возбудителя на фоне повышения внимания к природно-очаговым инфекциям в мире. Возбудитель анаплазмоза формирует морулы в нейтрофилах и поддерживает внутриклеточную персистенцию, перепрограммируя сигнальные и регуляторные пути клетки-хозяина, тем самым обходя механизмы врожденной антибактериальной защиты. Целью обзора является систематизация современных представлений о молекулярных механизмах патогенности A. phagocytophilum и его белках-эффекторах. Проанализированы оригинальные статьи и обзоры, отобранные в базах PubMed, Elsevier и CyberLeninka. Приоритетными являлись публикации за последние 10 лет, при этом фундаментальные работы, впервые описывающие возбудителя, клиническую характеристику Anaplasma и основные эффекторные механизмы, включались независимо от года публикации. Всего в обзор вошло 50 источников. Особое внимание уделено экспериментальным данным о белках AnkA, Ats-1 и AptA, об их взаимодействии с клеточными мишенями и влиянии на апоптоз, транскрипцию, митохондриальные и сигнальные пути. Рассмотрен механизм выживания A. phagocytophilum в организме хозяина, заключающийся во внедрении возбудителя в клетки иммунной системы и изменении их функционирования. С помощью белков AnkA, Ats-1 и AptA бактерия подавляет естественную гибель клеток (апоптоз), блокирует выработку активных форм кислорода и нарушает передачу сигнала между белками внутри клетки. Эти эффекты позволяют патогену длительно сохраняться в организме, избегая уничтожения иммунной системой. Патогенные белки доставляются в клетку через систему секреции IV типа, характерную для ряда внутриклеточных возбудителей. Понимание роли эффекторных белков A. phagocytophilum в патогенезе анаплазмоза может стать основой для разработки новых методов диагностики данного заболевания, таргетной терапии и эпидемиологического надзора, особенно в регионах с природной очаговостью.</p>
      </abstract>
      <trans-abstract xml:lang="en">
        <p>Human granulocytic anaplasmosis is a natural-focal vector-borne infection caused by the obligate intracellular pathogen Anaplasma phagocytophilum. The relevance of this study is due to the growing interest in the pathogenesis of anaplasmosis and the virulence factors of its causative agent amid increasing attention to natural- focal infections worldwide. The pathogen forms morulae in neutrophils and maintains intracellular persistence by reprogramming host cell signaling and regulatory pathways, thereby bypassing innate antibacterial defense mechanisms. The aim of this review is to systematize current concepts of the molecular mechanisms of A. phagocytophilum pathogenicity and its effector proteins. Original articles and reviews, selected from the PubMed, Elsevier, and CyberLeninka databases, are analyzed. Priority is given to publications over the last 10 years, while fundamental studies that first described the pathogen, the clinical characteristics of Anaplasma infection, and key effector mechanisms are included regardless of the date of publication. A total of 50 sources are included in the review. Particular attention is paid to experimental data on the AnkA, Ats-1, and AptA proteins, their interactions with cellular targets, and their effects on apoptosis, transcription, mitochondrial pathways, and signaling pathways. The mechanism of A. phagocytophilum survival in the host is considered, which involves the invasion of immune system cells and alteration of their functioning. Using the AnkA, Ats-1, and AptA proteins, the bacterium suppresses natural cell death (apoptosis), blocks the production of reactive oxygen species, and disrupts intracellular protein signaling. This enables the pathogen to persist in the host for a long time while avoiding elimination by the immune system. Pathogenic proteins are delivered into the host cell via the type IV secretion system, which is characteristic of a number of intracellular pathogens. Understanding the role of A. phagocytophilum effector proteins in the pathogenesis of anaplasmosis may provide a basis for the development of new diagnostic methods for this disease, targeted therapy, and epidemiological surveillance, especially in regions with natural nidality.</p>
      </trans-abstract>
      <kwd-group xml:lang="ru">
        <title>Ключевые слова</title>
        <kwd>Anaplasma phagocytophilum</kwd>
        <kwd>гранулоцитарный анаплазмоз человека</kwd>
        <kwd>нейтрофилы</kwd>
        <kwd>система секреции IV типа</kwd>
        <kwd>белки-эффекторы</kwd>
        <kwd>внутриклеточная персистенция</kwd>
        <kwd>апоптоз</kwd>
        <kwd>аутофагия</kwd>
      </kwd-group>
      <kwd-group xml:lang="en">
        <title>Keywords</title>
        <kwd>Anaplasma phagocytophilum</kwd>
        <kwd>electroneuromyography</kwd>
        <kwd>neutrophil</kwd>
        <kwd>type IV secretion  system</kwd>
        <kwd>effector proteins</kwd>
        <kwd>intracellular persistence</kwd>
        <kwd>apoptosis</kwd>
        <kwd>autophagy</kwd>
      </kwd-group>
    </article-meta>
  </front>
  <body/>
  <back>
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